Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
Microtubule-associated proteins that are mainly expressed in neurons. Tau proteins constitute several isoforms and play an important role in the assembly of tubulin monomers into microtubules and in maintaining the cytoskeleton and axonal transport. Aggregation of specific sets of tau proteins in filamentous inclusions is the common feature of intraneuronal and glial fibrillar lesions (NEUROFIBRILLARY TANGLES; NEUROPIL THREADS) in numerous neurodegenerative disorders (ALZHEIMER DISEASE; TAUOPATHIES).
A familial disorder inherited as an autosomal dominant trait and characterized by the onset of progressive CHOREA and DEMENTIA in the fourth or fifth decade of life. Common initial manifestations include paranoia; poor impulse control; DEPRESSION; HALLUCINATIONS; and DELUSIONS. Eventually intellectual impairment; loss of fine motor control; ATHETOSIS; and diffuse chorea involving axial and limb musculature develops, leading to a vegetative state within 10-15 years of disease onset. The juvenile variant has a more fulminant course including SEIZURES; ATAXIA; dementia; and chorea. (From Adams et al., Principles of Neurology, 6th ed, pp1060-4)
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
A synuclein that is a major component of LEWY BODIES that plays a role in neurodegeneration and neuroprotection.
'Nerve tissue proteins' are specialized proteins found within the nervous system's biological tissue, including neurofilaments, neuronal cytoskeletal proteins, and neural cell adhesion molecules, which facilitate structural support, intracellular communication, and synaptic connectivity essential for proper neurological function.
Neurodegenerative disorders involving deposition of abnormal tau protein isoforms (TAU PROTEINS) in neurons and glial cells in the brain. Pathological aggregations of tau proteins are associated with mutation of the tau gene on chromosome 17 in patients with ALZHEIMER DISEASE; DEMENTIA; PARKINSONIAN DISORDERS; progressive supranuclear palsy (SUPRANUCLEAR PALSY, PROGRESSIVE); and corticobasal degeneration.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A generic term for any circumscribed mass of foreign (e.g., lead or viruses) or metabolically inactive materials (e.g., ceroid or MALLORY BODIES), within the cytoplasm or nucleus of a cell. Inclusion bodies are in cells infected with certain filtrable viruses, observed especially in nerve, epithelial, or endothelial cells. (Stedman, 25th ed)
Inherited disorders characterized by progressive atrophy and dysfunction of anatomically or physiologically related neurologic systems.
Disorders caused by imbalances in the protein homeostasis network - synthesis, folding, and transport of proteins; post-translational modifications; and degradation or clearance of misfolded proteins.
The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.
Small proteinaceous infectious particles which resist inactivation by procedures that modify NUCLEIC ACIDS and contain an abnormal isoform of a cellular protein which is a major and necessary component. The abnormal (scrapie) isoform is PrPSc (PRPSC PROTEINS) and the cellular isoform PrPC (PRPC PROTEINS). The primary amino acid sequence of the two isoforms is identical. Human diseases caused by prions include CREUTZFELDT-JAKOB SYNDROME; GERSTMANN-STRAUSSLER SYNDROME; and INSOMNIA, FATAL FAMILIAL.
A group of genetic, infectious, or sporadic degenerative human and animal nervous system disorders associated with abnormal PRIONS. These diseases are characterized by conversion of the normal prion protein to an abnormal configuration via a post-translational process. In humans, these conditions generally feature DEMENTIA; ATAXIA; and a fatal outcome. Pathologic features include a spongiform encephalopathy without evidence of inflammation. The older literature occasionally refers to these as unconventional SLOW VIRUS DISEASES. (From Proc Natl Acad Sci USA 1998 Nov 10;95(23):13363-83)
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A family of homologous proteins of low MOLECULAR WEIGHT that are predominately expressed in the BRAIN and that have been implicated in a variety of human diseases. They were originally isolated from CHOLINERGIC FIBERS of TORPEDO.
Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.
A group of dominantly inherited, predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. Progressive ataxia is a central feature of these conditions, and in certain subtypes POLYNEUROPATHY; DYSARTHRIA; visual loss; and other disorders may develop. (From Joynt, Clinical Neurology, 1997, Ch65, pp 12-17; J Neuropathol Exp Neurol 1998 Jun;57(6):531-43)
Heterogeneous group of neurodegenerative disorders characterized by frontal and temporal lobe atrophy associated with neuronal loss, gliosis, and dementia. Patients exhibit progressive changes in social, behavioral, and/or language function. Multiple subtypes or forms are recognized based on presence or absence of TAU PROTEIN inclusions. FTLD includes three clinical syndromes: FRONTOTEMPORAL DEMENTIA, semantic dementia, and PRIMARY PROGRESSIVE NONFLUENT APHASIA.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
An increased number of contiguous trinucleotide repeats in the DNA sequence from one generation to the next. The presence of these regions is associated with diseases such as FRAGILE X SYNDROME and MYOTONIC DYSTROPHY. Some CHROMOSOME FRAGILE SITES are composed of sequences where trinucleotide repeat expansion occurs.
The most common clinical form of FRONTOTEMPORAL LOBAR DEGENERATION, this dementia presents with personality and behavioral changes often associated with disinhibition, apathy, and lack of insight.
An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts. Clinical manifestations include GAIT ATAXIA, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. Most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin. (From Adams et al., Principles of Neurology, 6th ed, p1081; N Engl J Med 1996 Oct 17;335(16):1169-75) The severity of Friedreich ataxia associated with expansion of GAA repeats in the first intron of the frataxin gene correlates with the number of trinucleotide repeats. (From Durr et al, N Engl J Med 1996 Oct 17;335(16):1169-75)
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
The segregation and degradation of damaged or unwanted cytoplasmic constituents by autophagic vacuoles (cytolysosomes) composed of LYSOSOMES containing cellular components in the process of digestion; it plays an important role in BIOLOGICAL METAMORPHOSIS of amphibians, in the removal of bone by osteoclasts, and in the degradation of normal cell components in nutritional deficiency states.
A group of severe neurodegenerative diseases characterized by intracellular accumulation of autofluorescent wax-like lipid materials (CEROID; LIPOFUSCIN) in neurons. There are several subtypes based on mutations of the various genes, time of disease onset, and severity of the neurological defects such as progressive DEMENTIA; SEIZURES; and visual failure.
An island in Micronesia, east of the Philippines, the largest and southernmost of the Marianas. Its capital is Agana. It was discovered by Magellan in 1521 and occupied by Spain in 1565. They ceded it to the United States in 1898. It is an unincorporated territory of the United States, administered by the Department of the Interior since 1950. The derivation of the name Guam is in dispute. (From Webster's New Geographical Dictionary, 1988, p471)
A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.
Processes involved in the formation of TERTIARY PROTEIN STRUCTURE.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Abnormal structures located in various parts of the brain and composed of dense arrays of paired helical filaments (neurofilaments and microtubules). These double helical stacks of transverse subunits are twisted into left-handed ribbon-like filaments that likely incorporate the following proteins: (1) the intermediate filaments: medium- and high-molecular-weight neurofilaments; (2) the microtubule-associated proteins map-2 and tau; (3) actin; and (4) UBIQUITINS. As one of the hallmarks of ALZHEIMER DISEASE, the neurofibrillary tangles eventually occupy the whole of the cytoplasm in certain classes of cell in the neocortex, hippocampus, brain stem, and diencephalon. The number of these tangles, as seen in post mortem histology, correlates with the degree of dementia during life. Some studies suggest that tangle antigens leak into the systemic circulation both in the course of normal aging and in cases of Alzheimer disease.
A neurodegenerative disease characterized by dementia, mild parkinsonism, and fluctuations in attention and alertness. The neuropsychiatric manifestations tend to precede the onset of bradykinesia, MUSCLE RIGIDITY, and other extrapyramidal signs. DELUSIONS and visual HALLUCINATIONS are relatively frequent in this condition. Histologic examination reveals LEWY BODIES in the CEREBRAL CORTEX and BRAIN STEM. SENILE PLAQUES and other pathologic features characteristic of ALZHEIMER DISEASE may also be present. (From Neurology 1997;48:376-380; Neurology 1996;47:1113-1124)
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Intracytoplasmic, eosinophilic, round to elongated inclusions found in vacuoles of injured or fragmented neurons. The presence of Lewy bodies is the histological marker of the degenerative changes in LEWY BODY DISEASE and PARKINSON DISEASE but they may be seen in other neurological conditions. They are typically found in the substantia nigra and locus coeruleus but they are also seen in the basal forebrain, hypothalamic nuclei, and neocortex.
The directed transport of ORGANELLES and molecules along nerve cell AXONS. Transport can be anterograde (from the cell body) or retrograde (toward the cell body). (Alberts et al., Molecular Biology of the Cell, 3d ed, pG3)
The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.
Microsatellite repeats consisting of three nucleotides dispersed in the euchromatic arms of chromosomes.
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)
A degenerative disease of the central nervous system characterized by balance difficulties; OCULAR MOTILITY DISORDERS (supranuclear ophthalmoplegia); DYSARTHRIA; swallowing difficulties; and axial DYSTONIA. Onset is usually in the fifth decade and disease progression occurs over several years. Pathologic findings include neurofibrillary degeneration and neuronal loss in the dorsal MESENCEPHALON; SUBTHALAMIC NUCLEUS; RED NUCLEUS; pallidum; dentate nucleus; and vestibular nuclei. (From Adams et al., Principles of Neurology, 6th ed, pp1076-7)
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.
Neurons which activate MUSCLE CELLS.
A highly conserved 76-amino acid peptide universally found in eukaryotic cells that functions as a marker for intracellular PROTEIN TRANSPORT and degradation. Ubiquitin becomes activated through a series of complicated steps and forms an isopeptide bond to lysine residues of specific proteins within the cell. These "ubiquitinated" proteins can be recognized and degraded by proteosomes or be transported to specific compartments within the cell.
Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
A plant genus of the family Cycadaceae, order Cycadales, class Cycadopsida, division CYCADOPHYTA of palm-like trees. It is a source of CYCASIN, the beta-D-glucoside of methylazoxymethanol.
Proteins that specifically bind to IRON.
A large multisubunit complex that plays an important role in the degradation of most of the cytosolic and nuclear proteins in eukaryotic cells. It contains a 700-kDa catalytic sub-complex and two 700-kDa regulatory sub-complexes. The complex digests ubiquitinated proteins and protein activated via ornithine decarboxylase antizyme.
A group of disorders marked by progressive degeneration of motor neurons in the spinal cord resulting in weakness and muscular atrophy, usually without evidence of injury to the corticospinal tracts. Diseases in this category include Werdnig-Hoffmann disease and later onset SPINAL MUSCULAR ATROPHIES OF CHILDHOOD, most of which are hereditary. (Adams et al., Principles of Neurology, 6th ed, p1089)
The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
A rare form of DEMENTIA that is sometimes familial. Clinical features include APHASIA; APRAXIA; CONFUSION; ANOMIA; memory loss; and personality deterioration. This pattern is consistent with the pathologic findings of circumscribed atrophy of the poles of the FRONTAL LOBE and TEMPORAL LOBE. Neuronal loss is maximal in the HIPPOCAMPUS, entorhinal cortex, and AMYGDALA. Some ballooned cortical neurons contain argentophylic (Pick) bodies. (From Brain Pathol 1998 Apr;8(2):339-54; Adams et al., Principles of Neurology, 6th ed, pp1057-9)
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
A multifunctional heterogeneous-nuclear ribonucleoprotein that may play a role in homologous DNA pairing and recombination. The N-terminal portion of protein is a potent transcriptional activator, while the C terminus is required for RNA binding. The name FUS refers to the fact that genetic recombination events result in fusion oncogene proteins (ONCOGENE PROTEINS, FUSION) that contain the N-terminal region of this protein. These fusion proteins have been found in myxoid liposarcoma (LIPOSARCOMA, MYXOID) and acute myeloid leukemia.
The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.
Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
A syndrome complex composed of three conditions which represent clinical variants of the same disease process: STRIATONIGRAL DEGENERATION; SHY-DRAGER SYNDROME; and the sporadic form of OLIVOPONTOCEREBELLAR ATROPHIES. Clinical features include autonomic, cerebellar, and basal ganglia dysfunction. Pathologic examination reveals atrophy of the basal ganglia, cerebellum, pons, and medulla, with prominent loss of autonomic neurons in the brain stem and spinal cord. (From Adams et al., Principles of Neurology, 6th ed, p1076; Baillieres Clin Neurol 1997 Apr;6(1):187-204; Med Clin North Am 1999 Mar;83(2):381-92)
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
ANIMALS whose GENOME has been altered by GENETIC ENGINEERING, or their offspring.
The black substance in the ventral midbrain or the nucleus of cells containing the black substance. These cells produce DOPAMINE, an important neurotransmitter in regulation of the sensorimotor system and mood. The dark colored MELANIN is a by-product of dopamine synthesis.
A family of cellular proteins that mediate the correct assembly or disassembly of polypeptides and their associated ligands. Although they take part in the assembly process, molecular chaperones are not components of the final structures.
Abnormal isoform of prion proteins (PRIONS) resulting from a posttranslational modification of the cellular prion protein (PRPC PROTEINS). PrPSc are disease-specific proteins seen in certain human and animal neurodegenerative diseases (PRION DISEASES).
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A synuclein that is closely related to ALPHA-SYNUCLEIN. It may play a neuroprotective role against some of the toxic effects of aggregated ALPHA-SYNUCLEIN.
A performance test based on forced MOTOR ACTIVITY on a rotating rod, usually by a rodent. Parameters include the riding time (seconds) or endurance. Test is used to evaluate balance and coordination of the subjects, particular in experimental animal models for neurological disorders and drug effects.
Diamino acids are a type of modified amino acids containing two amino groups, which can be found in various biological molecules and play important roles in various cellular processes, such as nitrogen fixation and protein synthesis.
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
Circumscribed masses of foreign or metabolically inactive materials, within the CELL NUCLEUS. Some are VIRAL INCLUSION BODIES.
An increase number of repeats of a genomic, tandemly repeated DNA sequence from one generation to the next.
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
Neurons whose primary neurotransmitter is DOPAMINE.
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
Diseases characterized by the presence of abnormally phosphorylated, ubiquitinated, and cleaved DNA-binding protein TDP-43 in affected brain and spinal cord. Inclusions of the pathologic protein in neurons and glia, without the presence of AMYLOID, is the major feature of these conditions, thus making these proteinopathies distinct from most other neurogenerative disorders in which protein misfolding leads to brain amyloidosis. Both frontotemporal lobar degeneration and AMYOTROPHIC LATERAL SCLEROSIS exhibit this common method of pathogenesis and thus they may represent two extremes of a continuous clinicopathological spectrum of one disease.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
A serine-threonine kinase that plays important roles in CELL DIFFERENTIATION; CELL MIGRATION; and CELL DEATH of NERVE CELLS. It is closely related to other CYCLIN-DEPENDENT KINASES but does not seem to participate in CELL CYCLE regulation.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Type III intermediate filament proteins that assemble into neurofilaments, the major cytoskeletal element in nerve axons and dendrites. They consist of three distinct polypeptides, the neurofilament triplet. Types I, II, and IV intermediate filament proteins form other cytoskeletal elements such as keratins and lamins. It appears that the metabolism of neurofilaments is disturbed in Alzheimer's disease, as indicated by the presence of neurofilament epitopes in the neurofibrillary tangles, as well as by the severe reduction of the expression of the gene for the light neurofilament subunit of the neurofilament triplet in brains of Alzheimer's patients. (Can J Neurol Sci 1990 Aug;17(3):302)
A single-pass type I membrane protein. It is cleaved by AMYLOID PRECURSOR PROTEIN SECRETASES to produce peptides of varying amino acid lengths. A 39-42 amino acid peptide, AMYLOID BETA-PEPTIDES is a principal component of the extracellular amyloid in SENILE PLAQUES.
A nonspecific term referring both to the pathologic finding of swelling of distal portions of axons in the brain and to disorders which feature this finding. Neuroaxonal dystrophy is seen in various genetic diseases, vitamin deficiencies, and aging. Infantile neuroaxonal dystrophy is an autosomal recessive disease characterized by arrested psychomotor development at 6 months to 2 years of age, ataxia, brain stem dysfunction, and quadriparesis. Juvenile and adult forms also occur. Pathologic findings include brain atrophy and widespread accumulation of axonal spheroids throughout the neuroaxis, peripheral nerves, and dental pulp. (From Davis & Robertson, Textbook of Neuropathology, 2nd ed, p927)
Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharynx, larynx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or PERIPHERAL NERVE DISEASES. Motor ataxia may be associated with CEREBELLAR DISEASES; CEREBRAL CORTEX diseases; THALAMIC DISEASES; BASAL GANGLIA DISEASES; injury to the RED NUCLEUS; and other conditions.
Established cell cultures that have the potential to propagate indefinitely.
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.
Normal cellular isoform of prion proteins (PRIONS) encoded by a chromosomal gene and found in normal and scrapie-infected brain tissue, and other normal tissue. PrPC are protease-sensitive proteins whose function is unknown. Posttranslational modification of PrPC into PrPSC leads to infectivity.
Traumatic injuries to the brain, cranial nerves, spinal cord, autonomic nervous system, or neuromuscular system, including iatrogenic injuries induced by surgical procedures.
A rare transmissible encephalopathy most prevalent between the ages of 50 and 70 years. Affected individuals may present with sleep disturbances, personality changes, ATAXIA; APHASIA, visual loss, weakness, muscle atrophy, MYOCLONUS, progressive dementia, and death within one year of disease onset. A familial form exhibiting autosomal dominant inheritance and a new variant CJD (potentially associated with ENCEPHALOPATHY, BOVINE SPONGIFORM) have been described. Pathological features include prominent cerebellar and cerebral cortical spongiform degeneration and the presence of PRIONS. (From N Engl J Med, 1998 Dec 31;339(27))
The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.
A dominantly-inherited ATAXIA first described in people of Azorean and Portuguese descent, and subsequently identified in Brazil, Japan, China, and Australia. This disorder is classified as one of the SPINOCEREBELLAR ATAXIAS (Type 3) and has been associated with a mutation of the MJD1 gene on chromosome 14. Clinical features include progressive ataxia, DYSARTHRIA, postural instability, nystagmus, eyelid retraction, and facial FASCICULATIONS. DYSTONIA is prominent in younger patients (referred to as Type I Machado-Joseph Disease). Type II features ataxia and ocular signs; Type III features MUSCULAR ATROPHY and a sensorimotor neuropathy; and Type IV features extrapyramidal signs combined with a sensorimotor neuropathy. (From Clin Neurosci 1995;3(1):17-22; Ann Neurol 1998 Mar;43(3):288-96)
A class of morphologically heterogeneous cytoplasmic particles in animal and plant tissues characterized by their content of hydrolytic enzymes and the structure-linked latency of these enzymes. The intracellular functions of lysosomes depend on their lytic potential. The single unit membrane of the lysosome acts as a barrier between the enzymes enclosed in the lysosome and the external substrate. The activity of the enzymes contained in lysosomes is limited or nil unless the vesicle in which they are enclosed is ruptured. Such rupture is supposed to be under metabolic (hormonal) control. (From Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
Compounds having the nitro group, -NO2, attached to carbon. When attached to nitrogen they are nitramines and attached to oxygen they are NITRATES.
Proteins that form the core of amyloid fibrils. For example, the core of amyloid A is formed from amyloid A protein, also known as serum amyloid A protein or SAA protein.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
An active neurotoxic metabolite of 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE. The compound reduces dopamine levels, inhibits the biosynthesis of catecholamines, depletes cardiac norepinephrine and inactivates tyrosine hydroxylase. These and other toxic effects lead to cessation of oxidative phosphorylation, ATP depletion, and cell death. The compound, which is related to PARAQUAT, has also been used as an herbicide.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Formation of NEURONS which involves the differentiation and division of STEM CELLS in which one or both of the daughter cells become neurons.
Disturbances in mental processes related to learning, thinking, reasoning, and judgment.
Biphasic dose responses of cells or organisms (including microorganisms) to an exogenous or intrinsic factor, in which the factor induces stimulatory or beneficial effects at low doses and inhibitory or adverse effects at high doses.
Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.
A heterogenous group of degenerative syndromes marked by progressive cerebellar dysfunction either in isolation or combined with other neurologic manifestations. Sporadic and inherited subtypes occur. Inheritance patterns include autosomal dominant, autosomal recessive, and X-linked.
Neurologic disorders caused by exposure to toxic substances through ingestion, injection, cutaneous application, or other method. This includes conditions caused by biologic, chemical, and pharmaceutical agents.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
A fatal disease of the nervous system in sheep and goats, characterized by pruritus, debility, and locomotor incoordination. It is caused by proteinaceous infectious particles called PRIONS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Degeneration of distal aspects of a nerve axon following injury to the cell body or proximal portion of the axon. The process is characterized by fragmentation of the axon and its MYELIN SHEATH.
A homolog of ALPHA-SYNUCLEIN that plays a role in neurofilament network integrity. It is overexpressed in a variety of human NEOPLASMS and may be involved in modulating AXON architecture during EMBRYONIC DEVELOPMENT and in the adult. Gamma-Synuclein may also activate SIGNAL TRANSDUCTION PATHWAYS associated with ETS-DOMAIN PROTEIN ELK-1.
A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.
Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.
A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.
Proteins produced from GENES that have acquired MUTATIONS.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
An autosomal recessive lipid storage disorder that is characterized by accumulation of CHOLESTEROL and SPHINGOMYELINS in cells of the VISCERA and the CENTRAL NERVOUS SYSTEM. Type C (or C1) and type D are allelic disorders caused by mutation of gene (NPC1) encoding a protein that mediate intracellular cholesterol transport from lysosomes. Clinical signs include hepatosplenomegaly and chronic neurological symptoms. Type D is a variant in people with a Nova Scotia ancestry.
Protein analogs and derivatives of the Aequorea victoria green fluorescent protein that emit light (FLUORESCENCE) when excited with ULTRAVIOLET RAYS. They are used in REPORTER GENES in doing GENETIC TECHNIQUES. Numerous mutants have been made to emit other colors or be sensitive to pH.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Peptide hydrolases that contain at the active site a SERINE residue involved in catalysis.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
An autosomal dominant disorder characterized by degeneration of the THALAMUS and progressive insomnia. It is caused by a mutation in the prion protein (PRIONS).
A genus of small, two-winged flies containing approximately 900 described species. These organisms are the most extensively studied of all genera from the standpoint of genetics and cytology.
A member of the nerve growth factor family of trophic factors. In the brain BDNF has a trophic action on retinal, cholinergic, and dopaminergic neurons, and in the peripheral nervous system it acts on both motor and sensory neurons. (From Kendrew, The Encyclopedia of Molecular Biology, 1994)
Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
The continuous remodeling of MITOCHONDRIA shape by fission and fusion in response to physiological conditions.
The use of silver, usually silver nitrate, as a reagent for producing contrast or coloration in tissue specimens.
A botanical insecticide that is an inhibitor of mitochondrial electron transport.
Thiolester hydrolases are enzymes that catalyze the hydrolysis of thioester bonds, commonly found in acetyl-CoA and other coenzyme A derivatives, to produce free carboxylic acids and CoASH.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
The observable response an animal makes to any situation.
Elements of limited time intervals, contributing to particular results or situations.
A group of inherited diseases that share similar phenotypes but are genetically diverse. Different genetic loci for autosomal recessive, autosomal dominant, and x-linked forms of hereditary spastic paraplegia have been identified. Clinically, patients present with slowly progressive distal limb weakness and lower extremity spasticity. Peripheral sensory neurons may be affected in the later stages of the disease. (J Neurol Neurosurg Psychiatry 1998 Jan;64(1):61-6; Curr Opin Neurol 1997 Aug;10(4):313-8)
The process by which chemical compounds provide protection to cells against harmful agents.
The assembly of the QUATERNARY PROTEIN STRUCTURE of multimeric proteins (MULTIPROTEIN COMPLEXES) from their composite PROTEIN SUBUNITS.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Self-renewing cells that generate the main phenotypes of the nervous system in both the embryo and adult. Neural stem cells are precursors to both NEURONS and NEUROGLIA.
Cleavage of proteins into smaller peptides or amino acids either by PROTEASES or non-enzymatically (e.g., Hydrolysis). It does not include Protein Processing, Post-Translational.
Electron microscopy in which the ELECTRONS or their reaction products that pass down through the specimen are imaged below the plane of the specimen.
The physical activity of a human or an animal as a behavioral phenomenon.
The output neurons of the cerebellar cortex.
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
A state in which attention is largely directed inward upon one's self.
A mutation in which a codon is mutated to one directing the incorporation of a different amino acid. This substitution may result in an inactive or unstable product. (From A Dictionary of Genetics, King & Stansfield, 5th ed)
A subclass of histone deacetylases that are NAD-dependent. Several members of the SIRTUINS family are included in this subclass.
Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.
The characteristic 3-dimensional shape and arrangement of multimeric proteins (aggregates of more than one polypeptide chain).
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
A species of fruit fly much used in genetics because of the large size of its chromosomes.
A cell line generated from human embryonic kidney cells that were transformed with human adenovirus type 5.
A diverse class of enzymes that interact with UBIQUITIN-CONJUGATING ENZYMES and ubiquitination-specific protein substrates. Each member of this enzyme group has its own distinct specificity for a substrate and ubiquitin-conjugating enzyme. Ubiquitin-protein ligases exist as both monomeric proteins multiprotein complexes.
The middle of the three primitive cerebral vesicles of the embryonic brain. Without further subdivision, midbrain develops into a short, constricted portion connecting the PONS and the DIENCEPHALON. Midbrain contains two major parts, the dorsal TECTUM MESENCEPHALI and the ventral TEGMENTUM MESENCEPHALI, housing components of auditory, visual, and other sensorimoter systems.
In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell.
Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury.
A metabolite of tryptophan with a possible role in neurodegenerative disorders. Elevated CSF levels of quinolinic acid are correlated with the severity of neuropsychological deficits in patients who have AIDS.
A division of GYMNOSPERMS which look like palm trees (ARECACEAE) but are more closely related to PINUS. They have large cones and large pinnate leaves and are sometimes called cycads, a term which may also refer more narrowly to cycadales or CYCAS.
A species of nematode that is widely used in biological, biochemical, and genetic studies.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
The transfer of STEM CELLS from one individual to another within the same species (TRANSPLANTATION, HOMOLOGOUS) or between species (XENOTRANSPLANTATION), or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). The source and location of the stem cells determines their potency or pluripotency to differentiate into various cell types.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Proteins that originate from insect species belonging to the genus DROSOPHILA. The proteins from the most intensely studied species of Drosophila, DROSOPHILA MELANOGASTER, are the subject of much interest in the area of MORPHOGENESIS and development.
An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC 1.14.16.2.
A class of large neuroglial (macroglial) cells in the central nervous system. Oligodendroglia may be called interfascicular, perivascular, or perineuronal (not the same as SATELLITE CELLS, PERINEURONAL of GANGLIA) according to their location. They form the insulating MYELIN SHEATH of axons in the central nervous system.
A progressive form of dementia characterized by the global loss of language abilities and initial preservation of other cognitive functions. Fluent and nonfluent subtypes have been described. Eventually a pattern of global cognitive dysfunction, similar to ALZHEIMER DISEASE, emerges. Pathologically, there are no Alzheimer or PICK DISEASE like changes, however, spongiform changes of cortical layers II and III are present in the TEMPORAL LOBE and FRONTAL LOBE. (From Brain 1998 Jan;121(Pt 1):115-26)
A heterogeneous group of primarily familial disorders characterized by myoclonic seizures, tonic-clonic seizures, ataxia, progressive intellectual deterioration, and neuronal degeneration. These include LAFORA DISEASE; MERRF SYNDROME; NEURONAL CEROID-LIPOFUSCINOSIS; sialidosis (see MUCOLIPIDOSES), and UNVERRICHT-LUNDBORG SYNDROME.
A metallic element with atomic symbol Fe, atomic number 26, and atomic weight 55.85. It is an essential constituent of HEMOGLOBINS; CYTOCHROMES; and IRON-BINDING PROTEINS. It plays a role in cellular redox reactions and in the transport of OXYGEN.
Mice which carry mutant genes for neurologic defects or abnormalities.
The biochemical and electrophysiological interactions between the NERVOUS SYSTEM and IMMUNE SYSTEM.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A class of MOLECULAR CHAPERONES found in both prokaryotes and in several compartments of eukaryotic cells. These proteins can interact with polypeptides during a variety of assembly processes in such a way as to prevent the formation of nonfunctional structures.
A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
The entire nerve apparatus, composed of a central part, the brain and spinal cord, and a peripheral part, the cranial and spinal nerves, autonomic ganglia, and plexuses. (Stedman, 26th ed)

Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: a neuroprotective role of inflammation? (1/2534)

Brain-derived neurotrophic factor (BDNF) has potent effects on neuronal survival and plasticity during development and after injury. In the nervous system, neurons are considered the major cellular source of BDNF. We demonstrate here that in addition, activated human T cells, B cells, and monocytes secrete bioactive BDNF in vitro. Notably, in T helper (Th)1- and Th2-type CD4(+) T cell lines specific for myelin autoantigens such as myelin basic protein or myelin oligodendrocyte glycoprotein, BDNF production is increased upon antigen stimulation. The BDNF secreted by immune cells is bioactive, as it supports neuronal survival in vitro. Using anti-BDNF monoclonal antibody and polyclonal antiserum, BDNF immunoreactivity is demonstrable in inflammatory infiltrates in the brain of patients with acute disseminated encephalitis and multiple sclerosis. The results raise the possibility that in the nervous system, inflammatory infiltrates have a neuroprotective effect, which may limit the success of nonselective immunotherapies.  (+info)

A new X linked neurodegenerative syndrome with mental retardation, blindness, convulsions, spasticity, mild hypomyelination, and early death maps to the pericentromeric region. (2/2534)

We report on a family with an X linked neurodegenerative disorder consisting of mental retardation, blindness, convulsions, spasticity, and early death. Neuropathological examination showed mild hypomyelination. By linkage analysis, the underlying genetic defect could be assigned to the pericentromeric region of the X chromosome with a maximum lod score of 3.30 at theta=0.0 for the DXS1204 locus with DXS337 and PGK1P1 as flanking markers.  (+info)

Increased neurodegeneration during ageing in mice lacking high-affinity nicotine receptors. (3/2534)

We have examined neuroanatomical, biochemical and endocrine parameters and spatial learning in mice lacking the beta2 subunit of the nicotinic acetylcholine receptor (nAChR) during ageing. Aged beta2(-/-) mutant mice showed region-specific alterations in cortical regions, including neocortical hypotrophy, loss of hippocampal pyramidal neurons, astro- and microgliosis and elevation of serum corticosterone levels. Whereas adult mutant and control animals performed well in the Morris maze, 22- to 24-month-old beta2(-/-) mice were significantly impaired in spatial learning. These data show that beta2 subunit-containing nAChRs can contribute to both neuronal survival and maintenance of cognitive performance during ageing. beta2(-/-) mice may thus serve as one possible animal model for some of the cognitive deficits and degenerative processes which take place during physiological ageing and in Alzheimer's disease, particularly those associated with dysfunction of the cholinergic system.  (+info)

Mitochondria in organismal aging and degeneration. (4/2534)

Several lines of experimentation support the view that the genetic, biochemical and bioenergetic functions of somatic mitochondria deteriorate during normal aging. Deletion mutations of the mitochondrial genome accumulate exponentially with age in nerve and muscle tissue of humans and multiple other species. In muscle, a tissue that undergoes age-related fiber loss and atrophy in humans, there is an exponential rise in the number of cytochrome-oxidase-deficient fibers, which is first detectable in the fourth decile of age. Most biochemical studies of animal mitochondrial activity indicate a decline in electron transport activity with age, as well as decreased bioenergetic capacity with age, as measured by mitochondrial membrane potential. Mitochondrial mutations may be both the result of mitochondrial oxidative stress, and cells bearing pure populations of pathogenic mitochondrial mutations are sensitized to oxidant stress. Oxidant stress to mitochondria is known to induce the mitochondrial permeability transition, which has recently been implicated in the release of cytochrome c and the initiation of apoptosis. Thus several lines of evidence support a contribution of mitochondrial dysfunction to the phenotypic changes associated with aging.  (+info)

Apoptosis in neurodegenerative diseases: the role of mitochondria. (5/2534)

Nerve cell death is the central feature of the human neurodegenerative diseases. It has long been thought that nerve cell death in these disorders occurs by way of necrosis, a process characterized by massive transmembrane ion currents, compromise of mitochondrial ATP production, and the formation of high levels of reactive oxygen species combining to induce rapid disruption of organelles, cell swelling, and plasma membrane rupture with a secondary inflammatory response. Nuclear DNA is relatively preserved. Recent evidence now indicates that the process of apoptosis rather than necrosis primarily contributes to nerve cell death in neurodegeneration. This has opened up new avenues for understanding the pathogenesis of neurodegeneration and may lead to new and more effective therapeutic approaches to these diseases.  (+info)

Nitric oxide, mitochondria and neurological disease. (6/2534)

Damage to the mitochondrial electron transport chain has been suggested to be an important factor in the pathogenesis of a range of neurological disorders, such as Parkinson's disease, Alzheimer's disease, multiple sclerosis, stroke and amyotrophic lateral sclerosis. There is also a growing body of evidence to implicate excessive or inappropriate generation of nitric oxide (NO) in these disorders. It is now well documented that NO and its toxic metabolite, peroxynitrite (ONOO-), can inhibit components of the mitochondrial respiratory chain leading, if damage is severe enough, to a cellular energy deficiency state. Within the brain, the susceptibility of different brain cell types to NO and ONOO- exposure may be dependent on factors such as the intracellular reduced glutathione (GSH) concentration and an ability to increase glycolytic flux in the face of mitochondrial damage. Thus neurones, in contrast to astrocytes, appear particularly vulnerable to the action of these molecules. Following cytokine exposure, astrocytes can increase NO generation, due to de novo synthesis of the inducible form of nitric oxide synthase (NOS). Whilst the NO/ONOO- so formed may not affect astrocyte survival, these molecules may diffuse out to cause mitochondrial damage, and possibly cell death, to other cells, such as neurones, in close proximity. Evidence is now available to support this scenario for neurological disorders, such as multiple sclerosis. In other conditions, such as ischaemia, increased availability of glutamate may lead to an activation of a calcium-dependent nitric oxide synthase associated with neurones. Such increased/inappropriate NO formation may contribute to energy depletion and neuronal cell death. The evidence available for NO/ONOO--mediated mitochondrial damage in various neurological disorders is considered and potential therapeutic strategies are proposed.  (+info)

Studies on the role of dopamine in the degeneration of 5-HT nerve endings in the brain of Dark Agouti rats following 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') administration. (7/2534)

1. We investigated whether dopamine plays a role in the neurodegeneration of 5-hydroxytryptamine (5-HT) nerve endings occurring in Dark Agouti rat brain after 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') administration. 2. Haloperidol (2 mg kg(-1) i.p.) injected 5 min prior and 55 min post MDMA (15 mg kg(-1) i.p.) abolished the acute MDMA-induced hyperthermia and attenuated the neurotoxic loss of 5-HT 7 days later. When the rectal temperature of MDMA + haloperidol treated rats was kept elevated, this protective effect was marginal. 3. MDMA (15 mg kg(-1)) increased the dopamine concentration in the dialysate from a striatal microdialysis probe by 800%. L-DOPA (25 mg kg(-1) i.p., plus benserazide, 6.25 mg kg(-1) i.p.) injected 2 h after MDMA (15 mg kg(-1)) enhanced the increase in dopamine in the dialysate, but subsequent neurodegeneration was unaltered. L-DOPA (25 mg kg(-1)) injected before a sub-toxic dose of MDMA (5 mg kg(-1)) failed to induce neurodegeneration. 4. The MDMA-induced increase in free radical formation in the hippocampus (indicated by increased 2,3- and 2,5-dihydroxybenzoic acid in a microdialysis probe perfused with salicylic acid) was unaltered by L-DOPA. 5. The neuroprotective drug clomethiazole (50 mg kg(-1) i.p.) did not influence the MDMA-induced increase in extracellular dopamine. 6. These data suggest that previous observations on the protective effect of haloperidol and potentiating effect of L-DOPA on MDMA-induced neurodegeneration may have resulted from effects on MDMA-induced hyperthermia. 7. The increased extracellular dopamine concentration following MDMA may result from effects of MDMA on dopamine re-uptake, monoamine oxidase and 5-HT release rather than an 'amphetamine-like' action on dopamine release, thus explaining why the drug does not induce degeneration of dopamine nerve endings.  (+info)

Possible role of NF-kappaB and p53 in the glutamate-induced pro-apoptotic neuronal pathway. (8/2534)

Apoptosis is now recognized as an important component in many progressive and acute neurodegenerative diseases. Extracellular signals and intracellular mechanisms triggering and regulating apoptosis in neuronal cells are still a matter of investigation. Here we review data from our and other laboratories with the aim to elucidate the nature of some proteins which are known to be involved in cell cycle regulation as well as in promoting degeneration and apoptosis of neurons. The following molecules will be taken into consideration: NF-kappaB, p53, p21 and MSH2. These proteins are activated by neurotoxic experimental conditions which involve the stimulation of selective receptors for the excitatory aminoacid glutamate. Thus, we hypothesize their contribution to an intracellular pathway responsible for the glutamate-induced neuronal death. Identification of such mechanisms could be relevant for understanding the apoptosis associated with various neurodegenerative diseases as well as for developing novel strategies of pharmacological intervention.  (+info)

Neurodegenerative diseases are a group of disorders characterized by progressive and persistent loss of neuronal structure and function, often leading to cognitive decline, functional impairment, and ultimately death. These conditions are associated with the accumulation of abnormal protein aggregates, mitochondrial dysfunction, oxidative stress, chronic inflammation, and genetic mutations in the brain. Examples of neurodegenerative diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, Amyotrophic Lateral Sclerosis (ALS), and Spinal Muscular Atrophy (SMA). The underlying causes and mechanisms of these diseases are not fully understood, and there is currently no cure for most neurodegenerative disorders. Treatment typically focuses on managing symptoms and slowing disease progression.

Nerve degeneration, also known as neurodegeneration, is the progressive loss of structure and function of neurons, which can lead to cognitive decline, motor impairment, and various other symptoms. This process occurs due to a variety of factors, including genetics, environmental influences, and aging. It is a key feature in several neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. The degeneration can affect any part of the nervous system, leading to different symptoms depending on the location and extent of the damage.

Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disorder that affects nerve cells in the brain and spinal cord responsible for controlling voluntary muscle movements, such as speaking, walking, breathing, and swallowing. The condition is characterized by the degeneration of motor neurons in the brain (upper motor neurons) and spinal cord (lower motor neurons), leading to their death.

The term "amyotrophic" comes from the Greek words "a" meaning no or negative, "myo" referring to muscle, and "trophic" relating to nutrition. When a motor neuron degenerates and can no longer send impulses to the muscle, the muscle becomes weak and eventually atrophies due to lack of use.

The term "lateral sclerosis" refers to the hardening or scarring (sclerosis) of the lateral columns of the spinal cord, which are primarily composed of nerve fibers that carry information from the brain to the muscles.

ALS is often called Lou Gehrig's disease, named after the famous American baseball player who was diagnosed with the condition in 1939. The exact cause of ALS remains unknown, but it is believed to involve a combination of genetic and environmental factors. There is currently no cure for ALS, and treatment primarily focuses on managing symptoms and maintaining quality of life.

The progression of ALS varies from person to person, with some individuals experiencing rapid decline over just a few years, while others may have a more slow-progressing form of the disease that lasts several decades. The majority of people with ALS die from respiratory failure within 3 to 5 years after the onset of symptoms. However, approximately 10% of those affected live for 10 or more years following diagnosis.

Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.

Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. It's the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.

The early signs of the disease include forgetting recent events or conversations. As the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to carry out everyday tasks.

Currently, there's no cure for Alzheimer's disease. However, treatments can temporarily slow the worsening of dementia symptoms and improve quality of life.

Tau proteins are a type of microtubule-associated protein (MAP) found primarily in neurons of the central nervous system. They play a crucial role in maintaining the stability and structure of microtubules, which are essential components of the cell's cytoskeleton. Tau proteins bind to and stabilize microtubules, helping to regulate their assembly and disassembly.

In Alzheimer's disease and other neurodegenerative disorders known as tauopathies, tau proteins can become abnormally hyperphosphorylated, leading to the formation of insoluble aggregates called neurofibrillary tangles (NFTs) within neurons. These aggregates disrupt the normal function of microtubules and contribute to the degeneration and death of nerve cells, ultimately leading to cognitive decline and other symptoms associated with these disorders.

Huntington Disease (HD) is a genetic neurodegenerative disorder that affects both cognitive and motor functions. It is characterized by the progressive loss of neurons in various areas of the brain, particularly in the striatum and cortex. The disease is caused by an autosomal dominant mutation in the HTT gene, which codes for the huntingtin protein. The most common mutation is a CAG repeat expansion in this gene, leading to the production of an abnormal form of the huntingtin protein that is toxic to nerve cells.

The symptoms of HD typically appear between the ages of 30 and 50, but they can start earlier or later in life. The early signs of HD may include subtle changes in mood, cognition, and coordination. As the disease progresses, individuals with HD experience uncontrolled movements (chorea), emotional disturbances, cognitive decline, and difficulties with communication and swallowing. Eventually, they become dependent on others for their daily needs and lose their ability to walk, talk, and care for themselves.

There is currently no cure for HD, but medications and therapies can help manage the symptoms of the disease and improve quality of life. Genetic testing is available to confirm the diagnosis and provide information about the risk of passing the disease on to future generations.

The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:

1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.

The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.

Parkinson's disease is a progressive neurodegenerative disorder that affects movement. It is characterized by the death of dopamine-producing cells in the brain, specifically in an area called the substantia nigra. The loss of these cells leads to a decrease in dopamine levels, which results in the motor symptoms associated with Parkinson's disease. These symptoms can include tremors at rest, stiffness or rigidity of the limbs and trunk, bradykinesia (slowness of movement), and postural instability (impaired balance and coordination). In addition to these motor symptoms, non-motor symptoms such as cognitive impairment, depression, anxiety, and sleep disturbances are also common in people with Parkinson's disease. The exact cause of Parkinson's disease is unknown, but it is thought to be a combination of genetic and environmental factors. There is currently no cure for Parkinson's disease, but medications and therapies can help manage the symptoms and improve quality of life.

Alpha-synuclein is a protein that is primarily found in neurons (nerve cells) in the brain. It is encoded by the SNCA gene and is abundantly expressed in presynaptic terminals, where it is believed to play a role in the regulation of neurotransmitter release.

In certain neurological disorders, including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, alpha-synuclein can form aggregates known as Lewy bodies and Lewy neurites. These aggregates are a pathological hallmark of these diseases and are believed to contribute to the death of nerve cells, leading to the symptoms associated with these disorders.

The precise function of alpha-synuclein is not fully understood, but it is thought to be involved in various cellular processes such as maintaining the structure of the presynaptic terminal, regulating synaptic vesicle trafficking and neurotransmitter release, and protecting neurons from stress.

Nerve tissue proteins are specialized proteins found in the nervous system that provide structural and functional support to nerve cells, also known as neurons. These proteins include:

1. Neurofilaments: These are type IV intermediate filaments that provide structural support to neurons and help maintain their shape and size. They are composed of three subunits - NFL (light), NFM (medium), and NFH (heavy).

2. Neuronal Cytoskeletal Proteins: These include tubulins, actins, and spectrins that provide structural support to the neuronal cytoskeleton and help maintain its integrity.

3. Neurotransmitter Receptors: These are specialized proteins located on the postsynaptic membrane of neurons that bind neurotransmitters released by presynaptic neurons, triggering a response in the target cell.

4. Ion Channels: These are transmembrane proteins that regulate the flow of ions across the neuronal membrane and play a crucial role in generating and transmitting electrical signals in neurons.

5. Signaling Proteins: These include enzymes, receptors, and adaptor proteins that mediate intracellular signaling pathways involved in neuronal development, differentiation, survival, and death.

6. Adhesion Proteins: These are cell surface proteins that mediate cell-cell and cell-matrix interactions, playing a crucial role in the formation and maintenance of neural circuits.

7. Extracellular Matrix Proteins: These include proteoglycans, laminins, and collagens that provide structural support to nerve tissue and regulate neuronal migration, differentiation, and survival.

Tauopathies are a group of neurodegenerative disorders that are characterized by the abnormal accumulation and aggregation of the microtubule-associated protein Tau in neurons and glial cells. These misfolded Tau proteins form insoluble inclusions, such as neurofibrillary tangles (NFTs) and neuropil threads, which are associated with the degeneration and loss of neurons in specific regions of the brain.

Tauopathies include several well-known diseases, such as Alzheimer's disease (AD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and frontotemporal dementia with Parkinsonism-17 (FTDP-17). The exact cause of Tauopathies remains unclear, but genetic mutations, environmental factors, or a combination of both may contribute to the development and progression of these disorders.

The accumulation of abnormal Tau aggregates is believed to play a central role in the neurodegenerative process, leading to cognitive decline, motor impairment, and other neurological symptoms associated with Tauopathies. The diagnosis of Tauopathies typically involves clinical evaluation, imaging studies, and sometimes postmortem examination of brain tissue. Currently, there are no effective disease-modifying treatments for Tauopathies, but ongoing research is focused on developing therapies that target Tau aggregation and clearance to slow down or halt the progression of these debilitating disorders.

Neuroprotective agents are substances that protect neurons or nerve cells from damage, degeneration, or death caused by various factors such as trauma, inflammation, oxidative stress, or excitotoxicity. These agents work through different mechanisms, including reducing the production of free radicals, inhibiting the release of glutamate (a neurotransmitter that can cause cell damage in high concentrations), promoting the growth and survival of neurons, and preventing apoptosis (programmed cell death). Neuroprotective agents have been studied for their potential to treat various neurological disorders, including stroke, traumatic brain injury, Parkinson's disease, Alzheimer's disease, and multiple sclerosis. However, more research is needed to fully understand their mechanisms of action and to develop effective therapies.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Inclusion bodies are abnormal, intracellular accumulations or aggregations of various misfolded proteins, protein complexes, or other materials within the cells of an organism. They can be found in various tissues and cell types and are often associated with several pathological conditions, including infectious diseases, neurodegenerative disorders, and genetic diseases.

Inclusion bodies can vary in size, shape, and location depending on the specific disease or condition. Some inclusion bodies have a characteristic appearance under the microscope, such as eosinophilic (pink) staining with hematoxylin and eosin (H&E) histological stain, while others may require specialized stains or immunohistochemical techniques to identify the specific misfolded proteins involved.

Examples of diseases associated with inclusion bodies include:

1. Infectious diseases: Some viral infections, such as HIV, hepatitis B and C, and herpes simplex virus, can lead to the formation of inclusion bodies within infected cells.
2. Neurodegenerative disorders: Several neurodegenerative diseases are characterized by the presence of inclusion bodies, including Alzheimer's disease (amyloid-beta plaques and tau tangles), Parkinson's disease (Lewy bodies), Huntington's disease (Huntingtin aggregates), and amyotrophic lateral sclerosis (TDP-43 and SOD1 inclusions).
3. Genetic diseases: Certain genetic disorders, such as Danon disease, neuronal intranuclear inclusion disease, and some lysosomal storage disorders, can also present with inclusion bodies due to the accumulation of abnormal proteins or metabolic products within cells.

The exact role of inclusion bodies in disease pathogenesis remains unclear; however, they are often associated with cellular dysfunction, oxidative stress, and increased inflammation, which can contribute to disease progression and neurodegeneration.

Heredodegenerative disorders of the nervous system are a group of inherited conditions that involve progressive degeneration of the nervous system over time. These disorders are caused by genetic mutations that affect the development and function of nerve cells in the brain and spinal cord. The symptoms and severity of these disorders can vary widely, depending on the specific condition and the location and extent of nerve cell damage.

Examples of heredodegenerative disorders of the nervous system include:

1. Huntington's disease: a genetic disorder that causes the progressive breakdown of nerve cells in the brain, leading to uncontrolled movements, emotional problems, and cognitive decline.
2. Friedreich's ataxia: an inherited disorder that affects the nerves and muscle coordination, causing symptoms such as difficulty walking, poor balance, and speech problems.
3. Spinal muscular atrophy: a genetic disorder that affects the motor neurons in the spinal cord, leading to muscle weakness and wasting.
4. Hereditary sensory and autonomic neuropathies: a group of inherited disorders that affect the nerves that control sensation and automatic functions such as heart rate and digestion.
5. Leukodystrophies: a group of genetic disorders that affect the white matter of the brain, leading to symptoms such as motor and cognitive decline, seizures, and vision loss.

Treatment for heredodegenerative disorders of the nervous system typically focuses on managing symptoms and improving quality of life. There is no cure for most of these conditions, but research is ongoing to develop new treatments and therapies that may help slow or stop the progression of nerve cell damage.

Proteostasis is the process by which cells regulate the proper functioning and folding of proteins within the body to maintain cellular homeostasis. A deficiency in proteostasis refers to an impairment in this regulatory process, leading to the accumulation of misfolded or aggregated proteins. This can result in various diseases, such as neurodegenerative disorders, cancer, and metabolic conditions.

Proteostasis deficiencies can occur due to genetic mutations, environmental factors, or aging, which can affect the function of protein quality control systems, including chaperones, the ubiquitin-proteasome system, and autophagy. These systems are responsible for recognizing and disposing of misfolded proteins, preventing their accumulation and subsequent toxicity.

In summary, proteostasis deficiencies refer to impairments in the regulation of protein homeostasis within cells, leading to the accumulation of misfolded or aggregated proteins and contributing to various diseases.

Microglia are a type of specialized immune cell found in the brain and spinal cord. They are part of the glial family, which provide support and protection to the neurons in the central nervous system (CNS). Microglia account for about 10-15% of all cells found in the CNS.

The primary role of microglia is to constantly survey their environment and eliminate any potentially harmful agents, such as pathogens, dead cells, or protein aggregates. They do this through a process called phagocytosis, where they engulf and digest foreign particles or cellular debris. In addition to their phagocytic function, microglia also release various cytokines, chemokines, and growth factors that help regulate the immune response in the CNS, promote neuronal survival, and contribute to synaptic plasticity.

Microglia can exist in different activation states depending on the nature of the stimuli they encounter. In a resting state, microglia have a small cell body with numerous branches that are constantly monitoring their surroundings. When activated by an injury, infection, or neurodegenerative process, microglia change their morphology and phenotype, retracting their processes and adopting an amoeboid shape to migrate towards the site of damage or inflammation. Based on the type of activation, microglia can release both pro-inflammatory and anti-inflammatory factors that contribute to either neuroprotection or neurotoxicity.

Dysregulation of microglial function has been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and Amyotrophic Lateral Sclerosis (ALS). Therefore, understanding the role of microglia in health and disease is crucial for developing novel therapeutic strategies to treat these conditions.

Prions are misfolded proteins that can induce other normal proteins to also adopt the misfolded shape, leading to the formation of aggregates. These abnormal prion protein aggregates are associated with a group of progressive neurodegenerative diseases known as transmissible spongiform encephalopathies (TSEs). Examples of TSEs include bovine spongiform encephalopathy (BSE or "mad cow disease") in cattle, variant Creutzfeldt-Jakob disease (vCJD) in humans, and scrapie in sheep. The misfolded prion proteins are resistant to degradation by proteases, which contributes to their accumulation and subsequent neuronal damage, ultimately resulting in spongiform degeneration of the brain and other neurological symptoms associated with TSEs.

Prion diseases, also known as transmissible spongiform encephalopathies (TSEs), are a group of progressive neurodegenerative disorders that affect both humans and animals. They are unique in that they are caused by prions, which are misfolded proteins rather than infectious agents like bacteria or viruses. These abnormal prions can cause other normal proteins to misfold and accumulate in the brain, leading to brain damage and neurodegeneration.

Prion diseases can be sporadic, inherited, or acquired. Sporadic forms occur without a known cause and are the most common type. Inherited prion diseases are caused by mutations in the PRNP gene and are often associated with a family history of the disease. Acquired prion diseases can result from exposure to contaminated food (as in variant Creutzfeldt-Jakob disease), medical procedures (iatrogenic Creutzfeldt-Jakob disease), or inherited forms of the disease that cause abnormal prions to be secreted in body fluids (like kuru).

Common prion diseases in humans include:

1. Creutzfeldt-Jakob disease (CJD) - sporadic, inherited, and acquired forms
2. Variant Creutzfeldt-Jakob disease (vCJD) - acquired form linked to consumption of contaminated beef products
3. Gerstmann-Sträussler-Scheinker syndrome (GSS) - inherited form
4. Fatal familial insomnia (FFI) - inherited form
5. Kuru - an acquired form that occurred in a isolated tribe due to cannibalistic practices, now eradicated

Prion diseases are characterized by rapidly progressing dementia, neurological symptoms, and motor dysfunction. There is no known cure for these diseases, and they are universally fatal.

Transgenic mice are genetically modified rodents that have incorporated foreign DNA (exogenous DNA) into their own genome. This is typically done through the use of recombinant DNA technology, where a specific gene or genetic sequence of interest is isolated and then introduced into the mouse embryo. The resulting transgenic mice can then express the protein encoded by the foreign gene, allowing researchers to study its function in a living organism.

The process of creating transgenic mice usually involves microinjecting the exogenous DNA into the pronucleus of a fertilized egg, which is then implanted into a surrogate mother. The offspring that result from this procedure are screened for the presence of the foreign DNA, and those that carry the desired genetic modification are used to establish a transgenic mouse line.

Transgenic mice have been widely used in biomedical research to model human diseases, study gene function, and test new therapies. They provide a valuable tool for understanding complex biological processes and developing new treatments for a variety of medical conditions.

Synucleins are a family of small, heat-stable, water-soluble proteins that are primarily expressed in neurons. They are involved in various cellular processes such as modulating synaptic plasticity, vesicle trafficking, and neurotransmitter release. The most well-known members of this family are alpha-synuclein, beta-synuclein, and gamma-synuclein.

Abnormal accumulation and aggregation of alpha-synuclein into insoluble fibrils called Lewy bodies and Lewy neurites are hallmark features of several neurodegenerative disorders, including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. These conditions are collectively referred to as synucleinopathies. The dysfunction and aggregation of alpha-synuclein are thought to contribute to the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, a region of the brain involved in motor control, leading to the characteristic symptoms observed in these disorders.

Amyloid beta-peptides (Aβ) are small protein fragments that are crucially involved in the pathogenesis of Alzheimer's disease. They are derived from a larger transmembrane protein called the amyloid precursor protein (APP) through a series of proteolytic cleavage events.

The two primary forms of Aβ peptides are Aβ40 and Aβ42, which differ in length by two amino acids. While both forms can be harmful, Aβ42 is more prone to aggregation and is considered to be the more pathogenic form. These peptides have the tendency to misfold and accumulate into oligomers, fibrils, and eventually insoluble plaques that deposit in various areas of the brain, most notably the cerebral cortex and hippocampus.

The accumulation of Aβ peptides is believed to initiate a cascade of events leading to neuroinflammation, oxidative stress, synaptic dysfunction, and neuronal death, which are all hallmarks of Alzheimer's disease. Although the exact role of Aβ in the onset and progression of Alzheimer's is still under investigation, it is widely accepted that they play a central part in the development of this debilitating neurodegenerative disorder.

Spinocerebellar ataxias (SCAs) are a group of genetic disorders that affect the cerebellum, which is the part of the brain responsible for coordinating muscle movements. SCAs are characterized by progressive problems with balance, speech, and coordination. They are caused by mutations in various genes that result in the production of abnormal proteins that accumulate in neurons, leading to their degeneration.

There are over 40 different types of SCAs, each caused by a different genetic mutation. Some of the more common types include SCA1, SCA2, SCA3, SCA6, and SCA7. The symptoms and age of onset can vary widely depending on the type of SCA.

In addition to problems with coordination and balance, people with SCAs may also experience muscle weakness, stiffness, tremors, spasticity, and difficulty swallowing or speaking. Some types of SCAs can also cause visual disturbances, hearing loss, and cognitive impairment. Currently, there is no cure for SCAs, but treatments such as physical therapy, speech therapy, and medications can help manage the symptoms.

Frontotemporal lobar degeneration (FTLD) is a group of disorders characterized by the progressive degeneration of the frontal and temporal lobes of the brain. These areas of the brain are involved in decision-making, behavior, emotion, and language. FTLD can be divided into several subtypes based on the specific clinical features and the underlying protein abnormalities.

The three main subtypes of FTLD are:

1. Behavioral variant frontotemporal dementia (bvFTD): This subtype is characterized by changes in personality, behavior, and judgment. People with bvFTD may lose their social inhibitions, become impulsive, or develop compulsive behaviors. They may also have difficulty with emotional processing and empathy.
2. Primary progressive aphasia (PPA): This subtype is characterized by the gradual deterioration of language skills. People with PPA may have difficulty speaking, understanding spoken or written language, or both. There are three subtypes of PPA: nonfluent/agrammatic variant, semantic variant, and logopenic variant.
3. Motor neuron disease (MND) with FTLD: This subtype is characterized by the degeneration of motor neurons, which are the nerve cells responsible for controlling voluntary muscle movements. People with MND with FTLD may develop symptoms of amyotrophic lateral sclerosis (ALS), such as muscle weakness, stiffness, and twitching, as well as cognitive and behavioral changes associated with FTLD.

The underlying protein abnormalities in FTLD include:

1. Tau protein: In some forms of FTLD, the tau protein accumulates and forms clumps called tangles inside nerve cells. This is also seen in Alzheimer's disease.
2. TDP-43 protein: In other forms of FTLD, the TDP-43 protein accumulates and forms clumps inside nerve cells.
3. Fused in sarcoma (FUS) protein: In a small number of cases, the FUS protein accumulates and forms clumps inside nerve cells.

FTLD is typically a progressive disorder, meaning that symptoms worsen over time. There is currently no cure for FTLD, but there are treatments available to help manage symptoms and improve quality of life.

Cell death is the process by which cells cease to function and eventually die. There are several ways that cells can die, but the two most well-known and well-studied forms of cell death are apoptosis and necrosis.

Apoptosis is a programmed form of cell death that occurs as a normal and necessary process in the development and maintenance of healthy tissues. During apoptosis, the cell's DNA is broken down into small fragments, the cell shrinks, and the membrane around the cell becomes fragmented, allowing the cell to be easily removed by phagocytic cells without causing an inflammatory response.

Necrosis, on the other hand, is a form of cell death that occurs as a result of acute tissue injury or overwhelming stress. During necrosis, the cell's membrane becomes damaged and the contents of the cell are released into the surrounding tissue, causing an inflammatory response.

There are also other forms of cell death, such as autophagy, which is a process by which cells break down their own organelles and proteins to recycle nutrients and maintain energy homeostasis, and pyroptosis, which is a form of programmed cell death that occurs in response to infection and involves the activation of inflammatory caspases.

Cell death is an important process in many physiological and pathological processes, including development, tissue homeostasis, and disease. Dysregulation of cell death can contribute to the development of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases.

Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Trinucleotide Repeat Expansion is a genetic mutation where a sequence of three DNA nucleotides is repeated more frequently than what is typically found in the general population. In this type of mutation, the number of repeats can expand or increase from one generation to the next, leading to an increased risk of developing certain genetic disorders.

These disorders are often neurological and include conditions such as Huntington's disease, myotonic dystrophy, fragile X syndrome, and Friedreich's ataxia. The severity of these diseases can be related to the number of repeats present in the affected gene, with a higher number of repeats leading to more severe symptoms or an earlier age of onset.

It is important to note that not all trinucleotide repeat expansions will result in disease, and some people may carry these mutations without ever developing any symptoms. However, if the number of repeats crosses a certain threshold, it can lead to genetic instability and an increased risk of disease development.

Frontotemporal dementia (FTD) is a group of disorders caused by progressive degeneration of the frontal and temporal lobes of the brain. These areas of the brain are associated with personality, behavior, and language.

There are three main types of FTD:

1. Behavioral variant FTD (bvFTD): This type is characterized by changes in personality, behavior, and judgment. Individuals may become socially inappropriate, emotionally indifferent, or impulsive. They may lose interest in things they used to enjoy and have difficulty with tasks that require planning and organization.

2. Primary progressive aphasia (PPA): This type affects language abilities. There are two main subtypes of PPA: semantic dementia and progressive nonfluent aphasia. Semantic dementia is characterized by difficulty understanding words and objects, while progressive nonfluent aphasia is characterized by problems with speech production and articulation.

3. Motor neuron disease (MND) associated FTD: Some individuals with FTD may also develop motor neuron disease, which affects the nerves that control muscle movement. This can lead to weakness, stiffness, and wasting of muscles, as well as difficulty swallowing and speaking.

FTD is a degenerative disorder, meaning that symptoms get worse over time. There is no cure for FTD, but there are treatments available to help manage symptoms and improve quality of life. The exact cause of FTD is not known, but it is believed to be related to abnormalities in certain proteins in the brain. In some cases, FTD may run in families and be caused by genetic mutations.

Friedreich Ataxia is a genetic disorder that affects the nervous system and causes issues with movement. It is characterized by progressive damage to the nerves (neurons) in the spinal cord and peripheral nerves, which can lead to problems with muscle coordination, gait, speech, and hearing. The condition is also associated with heart disorders, diabetes, and vision impairment.

Friedreich Ataxia is caused by a mutation in the FXN gene, which provides instructions for making a protein called frataxin. This protein plays a role in the production of energy within cells, particularly in the mitochondria. The mutation in the FXN gene leads to reduced levels of frataxin, which can cause nerve damage and other symptoms associated with Friedreich Ataxia.

The condition typically begins in childhood or early adulthood and progresses over time, often leading to significant disability. There is currently no cure for Friedreich Ataxia, but treatments are available to help manage the symptoms and improve quality of life.

Mitochondria are specialized structures located inside cells that convert the energy from food into ATP (adenosine triphosphate), which is the primary form of energy used by cells. They are often referred to as the "powerhouses" of the cell because they generate most of the cell's supply of chemical energy. Mitochondria are also involved in various other cellular processes, such as signaling, differentiation, and apoptosis (programmed cell death).

Mitochondria have their own DNA, known as mitochondrial DNA (mtDNA), which is inherited maternally. This means that mtDNA is passed down from the mother to her offspring through the egg cells. Mitochondrial dysfunction has been linked to a variety of diseases and conditions, including neurodegenerative disorders, diabetes, and aging.

Autophagy is a fundamental cellular process that involves the degradation and recycling of damaged or unnecessary cellular components, such as proteins and organelles. The term "autophagy" comes from the Greek words "auto" meaning self and "phagy" meaning eating. It is a natural process that occurs in all types of cells and helps maintain cellular homeostasis by breaking down and recycling these components.

There are several different types of autophagy, including macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Macroautophagy is the most well-known form and involves the formation of a double-membraned vesicle called an autophagosome, which engulfs the cellular component to be degraded. The autophagosome then fuses with a lysosome, an organelle containing enzymes that break down and recycle the contents of the autophagosome.

Autophagy plays important roles in various cellular processes, including adaptation to starvation, removal of damaged organelles, clearance of protein aggregates, and regulation of programmed cell death (apoptosis). Dysregulation of autophagy has been implicated in a number of diseases, including cancer, neurodegenerative disorders, and infectious diseases.

Neuronal Ceroid-Lipofuscinoses (NCLs) are a group of inherited neurodegenerative disorders characterized by the intracellular accumulation of autofluorescent lipopigment granules, known as ceroid-lipofuscin, in various tissues including the brain and retina. This accumulation is caused by mutations in different genes involved in lysosomal function or protein degradation pathways. The condition primarily affects neurons, leading to progressive neurological deterioration, including motor and cognitive decline, seizures, visual loss, and premature death. NCLs are also known as Batten disease, and they have several subtypes classified based on the age of onset, clinical presentation, and genetic defects.

I'm sorry for any confusion, but "Guam" is not a medical term. It is a territorial island in the Pacific Ocean and is an organized, unincorporated territory of the United States. Guam is known for its unique Chamorro culture, beautiful beaches, and historical sites. If you have any questions about medical terms or topics, I'd be happy to help with those instead!

Amyloid is a term used in medicine to describe abnormally folded protein deposits that can accumulate in various tissues and organs of the body. These misfolded proteins can form aggregates known as amyloid fibrils, which have a characteristic beta-pleated sheet structure. Amyloid deposits can be composed of different types of proteins, depending on the specific disease associated with the deposit.

In some cases, amyloid deposits can cause damage to organs and tissues, leading to various clinical symptoms. Some examples of diseases associated with amyloidosis include Alzheimer's disease (where amyloid-beta protein accumulates in the brain), systemic amyloidosis (where amyloid fibrils deposit in various organs such as the heart, kidneys, and liver), and type 2 diabetes (where amyloid deposits form in the pancreas).

It's important to note that not all amyloid deposits are harmful or associated with disease. However, when they do cause problems, treatment typically involves managing the underlying condition that is leading to the abnormal protein accumulation.

Aging is a complex, progressive and inevitable process of bodily changes over time, characterized by the accumulation of cellular damage and degenerative changes that eventually lead to increased vulnerability to disease and death. It involves various biological, genetic, environmental, and lifestyle factors that contribute to the decline in physical and mental functions. The medical field studies aging through the discipline of gerontology, which aims to understand the underlying mechanisms of aging and develop interventions to promote healthy aging and extend the human healthspan.

Dementia is a broad term that describes a decline in cognitive functioning, including memory, language, problem-solving, and judgment, severe enough to interfere with daily life. It is not a specific disease but rather a group of symptoms that may be caused by various underlying diseases or conditions. Alzheimer's disease is the most common cause of dementia, accounting for 60-80% of cases. Other causes include vascular dementia, Lewy body dementia, frontotemporal dementia, and Huntington's disease.

The symptoms of dementia can vary widely depending on the cause and the specific areas of the brain that are affected. However, common early signs of dementia may include:

* Memory loss that affects daily life
* Difficulty with familiar tasks
* Problems with language or communication
* Difficulty with visual and spatial abilities
* Misplacing things and unable to retrace steps
* Decreased or poor judgment
* Withdrawal from work or social activities
* Changes in mood or behavior

Dementia is a progressive condition, meaning that symptoms will gradually worsen over time. While there is currently no cure for dementia, early diagnosis and treatment can help slow the progression of the disease and improve quality of life for those affected.

Protein folding is the process by which a protein molecule naturally folds into its three-dimensional structure, following the synthesis of its amino acid chain. This complex process is determined by the sequence and properties of the amino acids, as well as various environmental factors such as temperature, pH, and the presence of molecular chaperones. The final folded conformation of a protein is crucial for its proper function, as it enables the formation of specific interactions between different parts of the molecule, which in turn define its biological activity. Protein misfolding can lead to various diseases, including neurodegenerative disorders such as Alzheimer's and Parkinson's disease.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Neurofibrillary tangles are a pathological hallmark of several neurodegenerative disorders, most notably Alzheimer's disease. They are intracellular inclusions composed of abnormally phosphorylated and aggregated tau protein, which forms paired helical filaments. These tangles accumulate within the neurons, leading to their dysfunction and eventual death. The presence and density of neurofibrillary tangles are strongly associated with cognitive decline and disease progression in Alzheimer's disease and other related dementias.

Lewy body disease, also known as dementia with Lewy bodies, is a type of progressive degenerative dementia that affects thinking, behavior, and movement. It's named after Dr. Friedrich Lewy, the scientist who discovered the abnormal protein deposits, called Lewy bodies, that are characteristic of this disease.

Lewy bodies are made up of a protein called alpha-synuclein and are found in the brain cells of individuals with Lewy body disease. These abnormal protein deposits are also found in people with Parkinson's disease, but they are more widespread in Lewy body disease, affecting multiple areas of the brain.

The symptoms of Lewy body disease can vary from person to person, but they often include:

* Cognitive decline, such as memory loss, confusion, and difficulty with problem-solving
* Visual hallucinations and delusions
* Parkinsonian symptoms, such as stiffness, tremors, and difficulty walking or moving
* Fluctuations in alertness and attention
* REM sleep behavior disorder, where a person acts out their dreams during sleep

Lewy body disease is a progressive condition, which means that the symptoms get worse over time. Currently, there is no cure for Lewy body disease, but medications can help manage some of the symptoms.

Astrocytes are a type of star-shaped glial cell found in the central nervous system (CNS), including the brain and spinal cord. They play crucial roles in supporting and maintaining the health and function of neurons, which are the primary cells responsible for transmitting information in the CNS.

Some of the essential functions of astrocytes include:

1. Supporting neuronal structure and function: Astrocytes provide structural support to neurons by ensheathing them and maintaining the integrity of the blood-brain barrier, which helps regulate the entry and exit of substances into the CNS.
2. Regulating neurotransmitter levels: Astrocytes help control the levels of neurotransmitters in the synaptic cleft (the space between two neurons) by taking up excess neurotransmitters and breaking them down, thus preventing excessive or prolonged activation of neuronal receptors.
3. Providing nutrients to neurons: Astrocytes help supply energy metabolites, such as lactate, to neurons, which are essential for their survival and function.
4. Modulating synaptic activity: Through the release of various signaling molecules, astrocytes can modulate synaptic strength and plasticity, contributing to learning and memory processes.
5. Participating in immune responses: Astrocytes can respond to CNS injuries or infections by releasing pro-inflammatory cytokines and chemokines, which help recruit immune cells to the site of injury or infection.
6. Promoting neuronal survival and repair: In response to injury or disease, astrocytes can become reactive and undergo morphological changes that aid in forming a glial scar, which helps contain damage and promote tissue repair. Additionally, they release growth factors and other molecules that support the survival and regeneration of injured neurons.

Dysfunction or damage to astrocytes has been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Peptides are short chains of amino acid residues linked by covalent bonds, known as peptide bonds. They are formed when two or more amino acids are joined together through a condensation reaction, which results in the elimination of a water molecule and the formation of an amide bond between the carboxyl group of one amino acid and the amino group of another.

Peptides can vary in length from two to about fifty amino acids, and they are often classified based on their size. For example, dipeptides contain two amino acids, tripeptides contain three, and so on. Oligopeptides typically contain up to ten amino acids, while polypeptides can contain dozens or even hundreds of amino acids.

Peptides play many important roles in the body, including serving as hormones, neurotransmitters, enzymes, and antibiotics. They are also used in medical research and therapeutic applications, such as drug delivery and tissue engineering.

Neurotoxins are substances that are poisonous or destructive to nerve cells (neurons) and the nervous system. They can cause damage by destroying neurons, disrupting communication between neurons, or interfering with the normal functioning of the nervous system. Neurotoxins can be produced naturally by certain organisms, such as bacteria, plants, and animals, or they can be synthetic compounds created in a laboratory. Examples of neurotoxins include botulinum toxin (found in botulism), tetrodotoxin (found in pufferfish), and heavy metals like lead and mercury. Neurotoxic effects can range from mild symptoms such as headaches, muscle weakness, and tremors, to more severe symptoms such as paralysis, seizures, and cognitive impairment. Long-term exposure to neurotoxins can lead to chronic neurological conditions and other health problems.

Parkinsonian disorders are a group of neurological conditions characterized by motor symptoms such as bradykinesia (slowness of movement), rigidity, resting tremor, and postural instability. These symptoms are caused by the degeneration of dopamine-producing neurons in the brain, particularly in the substantia nigra pars compacta.

The most common Parkinsonian disorder is Parkinson's disease (PD), which is a progressive neurodegenerative disorder. However, there are also several other secondary Parkinsonian disorders, including:

1. Drug-induced parkinsonism: This is caused by the use of certain medications, such as antipsychotics and metoclopramide.
2. Vascular parkinsonism: This is caused by small vessel disease in the brain, which can lead to similar symptoms as PD.
3. Dementia with Lewy bodies (DLB): This is a type of dementia that shares some features with PD, such as the presence of alpha-synuclein protein clumps called Lewy bodies.
4. Progressive supranuclear palsy (PSP): This is a rare brain disorder that affects movement, gait, and eye movements.
5. Multiple system atrophy (MSA): This is a progressive neurodegenerative disorder that affects multiple systems in the body, including the autonomic nervous system, motor system, and cerebellum.
6. Corticobasal degeneration (CBD): This is a rare neurological disorder that affects both movement and cognition.

It's important to note that while these disorders share some symptoms with PD, they have different underlying causes and may require different treatments.

Medical Definition:

Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of superoxide radicals (O2-) into oxygen (O2) and hydrogen peroxide (H2O2). This essential antioxidant defense mechanism helps protect the body's cells from damage caused by reactive oxygen species (ROS), which are produced during normal metabolic processes and can lead to oxidative stress when their levels become too high.

There are three main types of superoxide dismutase found in different cellular locations:
1. Copper-zinc superoxide dismutase (CuZnSOD or SOD1) - Present mainly in the cytoplasm of cells.
2. Manganese superoxide dismutase (MnSOD or SOD2) - Located within the mitochondrial matrix.
3. Extracellular superoxide dismutase (EcSOD or SOD3) - Found in the extracellular spaces, such as blood vessels and connective tissues.

Imbalances in SOD levels or activity have been linked to various pathological conditions, including neurodegenerative diseases, cancer, and aging-related disorders.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Biological models, also known as physiological models or organismal models, are simplified representations of biological systems, processes, or mechanisms that are used to understand and explain the underlying principles and relationships. These models can be theoretical (conceptual or mathematical) or physical (such as anatomical models, cell cultures, or animal models). They are widely used in biomedical research to study various phenomena, including disease pathophysiology, drug action, and therapeutic interventions.

Examples of biological models include:

1. Mathematical models: These use mathematical equations and formulas to describe complex biological systems or processes, such as population dynamics, metabolic pathways, or gene regulation networks. They can help predict the behavior of these systems under different conditions and test hypotheses about their underlying mechanisms.
2. Cell cultures: These are collections of cells grown in a controlled environment, typically in a laboratory dish or flask. They can be used to study cellular processes, such as signal transduction, gene expression, or metabolism, and to test the effects of drugs or other treatments on these processes.
3. Animal models: These are living organisms, usually vertebrates like mice, rats, or non-human primates, that are used to study various aspects of human biology and disease. They can provide valuable insights into the pathophysiology of diseases, the mechanisms of drug action, and the safety and efficacy of new therapies.
4. Anatomical models: These are physical representations of biological structures or systems, such as plastic models of organs or tissues, that can be used for educational purposes or to plan surgical procedures. They can also serve as a basis for developing more sophisticated models, such as computer simulations or 3D-printed replicas.

Overall, biological models play a crucial role in advancing our understanding of biology and medicine, helping to identify new targets for therapeutic intervention, develop novel drugs and treatments, and improve human health.

Lewy bodies are abnormal aggregates of alpha-synuclein protein that develop in nerve cells (neurons) in the brain. They are named after Frederick Lewy, a German-American neurologist who discovered them while working with Dr. Alois Alzheimer. The presence of Lewy bodies is a hallmark feature of Lewy body dementia, which includes both Parkinson's disease dementia and dementia with Lewy bodies.

Lewy bodies can lead to the dysfunction and death of neurons in areas of the brain that control movement, cognition, and behavior. This can result in a range of symptoms, including motor impairments, cognitive decline, visual hallucinations, and mood changes. The exact role of Lewy bodies in the development and progression of these disorders is not fully understood, but they are believed to contribute to the neurodegenerative process that underlies these conditions.

Axonal transport is the controlled movement of materials and organelles within axons, which are the nerve fibers of neurons (nerve cells). This intracellular transport system is essential for maintaining the structural and functional integrity of axons, particularly in neurons with long axonal processes. There are two types of axonal transport: anterograde transport, which moves materials from the cell body toward the synaptic terminals, and retrograde transport, which transports materials from the synaptic terminals back to the cell body. Anterograde transport is typically slower than retrograde transport and can be divided into fast and slow components based on velocity. Fast anterograde transport moves vesicles containing neurotransmitters and their receptors, as well as mitochondria and other organelles, at speeds of up to 400 mm/day. Slow anterograde transport moves cytoskeletal elements, proteins, and RNA at speeds of 1-10 mm/day. Retrograde transport is primarily responsible for recycling membrane components, removing damaged organelles, and transmitting signals from the axon terminal to the cell body. Dysfunctions in axonal transport have been implicated in various neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS).

The Central Nervous System (CNS) is the part of the nervous system that consists of the brain and spinal cord. It is called the "central" system because it receives information from, and sends information to, the rest of the body through peripheral nerves, which make up the Peripheral Nervous System (PNS).

The CNS is responsible for processing sensory information, controlling motor functions, and regulating various autonomic processes like heart rate, respiration, and digestion. The brain, as the command center of the CNS, interprets sensory stimuli, formulates thoughts, and initiates actions. The spinal cord serves as a conduit for nerve impulses traveling to and from the brain and the rest of the body.

The CNS is protected by several structures, including the skull (which houses the brain) and the vertebral column (which surrounds and protects the spinal cord). Despite these protective measures, the CNS remains vulnerable to injury and disease, which can have severe consequences due to its crucial role in controlling essential bodily functions.

Trinucleotide repeats refer to a specific type of DNA sequence expansion where a particular trinucleotide (a sequence made up of three nucleotides) is repeated multiple times. In normal genomic DNA, these repeats are usually present in a relatively stable and consistent range. However, when the number of repeats exceeds a certain threshold, it can result in an unstable genetic variant known as a trinucleotide repeat expansion.

These expansions can occur in various genes and are associated with several neurogenetic disorders, such as Huntington's disease, myotonic dystrophy, fragile X syndrome, and Friedreich's ataxia. The length of the trinucleotide repeat tends to expand further in subsequent generations, which can lead to anticipation – an earlier age of onset and increased severity of symptoms in successive generations.

The most common trinucleotide repeats involve CAG (cytosine-adenine-guanine) or CTG (cytosine-thymine-guanine) repeats, although other combinations like CGG, GAA, and GCT can also be involved. These repeat expansions can result in altered gene function, protein misfolding, aggregation, and toxicity, ultimately leading to the development of neurodegenerative diseases and other clinical manifestations.

Motor Neuron Disease (MND) is a progressive neurodegenerative disorder that affects the motor neurons, which are nerve cells in the brain and spinal cord responsible for controlling voluntary muscles involved in movement, speaking, breathing, and swallowing. As the motor neurons degenerate and die, they stop sending signals to the muscles, causing them to weaken, waste away (atrophy), and eventually lead to paralysis.

There are several types of MND, including:

1. Amyotrophic Lateral Sclerosis (ALS): Also known as Lou Gehrig's disease, this is the most common form of MND. It affects both upper and lower motor neurons, causing muscle weakness, stiffness, twitching, and atrophy throughout the body.
2. Progressive Bulbar Palsy (PBP): This type primarily affects the bulbar muscles in the brainstem, which control speech, swallowing, and chewing. Patients with PBP experience difficulties with speaking, slurred speech, and problems swallowing and may also have weak facial muscles and limb weakness.
3. Primary Lateral Sclerosis (PLS): This form of MND affects only the upper motor neurons, causing muscle stiffness, spasticity, and weakness, primarily in the legs. PLS progresses more slowly than ALS, and patients usually maintain their ability to speak and swallow for a longer period.
4. Progressive Muscular Atrophy (PMA): This type of MND affects only the lower motor neurons, causing muscle wasting, weakness, and fasciculations (muscle twitches). PMA progresses more slowly than ALS but can still be severely disabling over time.
5. Spinal Muscular Atrophy (SMA): This is a genetic form of MND that typically presents in infancy or childhood, although adult-onset forms exist. SMA affects the lower motor neurons in the spinal cord, causing muscle weakness and atrophy, primarily in the legs and trunk.

The exact cause of Motor Neuron Disease is not fully understood, but it is believed to involve a combination of genetic, environmental, and lifestyle factors. There is currently no cure for MND, and treatment focuses on managing symptoms, maintaining quality of life, and slowing disease progression through various therapies and medications.

Progressive Supranuclear Palsy (PSP) is a rare neurological disorder characterized by the progressive degeneration of brain cells that regulate movement, thoughts, behavior, and eye movements. The term "supranuclear" refers to the location of the damage in the brain, specifically above the level of the "nuclei" which are clusters of nerve cells that control voluntary movements.

The most common early symptom of PSP is a loss of balance and difficulty coordinating eye movements, particularly vertical gaze. Other symptoms may include stiffness or rigidity of muscles, slowness of movement, difficulty swallowing, changes in speech and writing, and cognitive decline leading to dementia.

PSP typically affects people over the age of 60, and its progression can vary from person to person. Currently, there is no cure for PSP, and treatment is focused on managing symptoms and maintaining quality of life.

Mitochondrial diseases are a group of disorders caused by dysfunctions in the mitochondria, which are the energy-producing structures in cells. These diseases can affect people of any age and can manifest in various ways, depending on which organs or systems are affected. Common symptoms include muscle weakness, neurological problems, cardiac disease, diabetes, and vision/hearing loss. Mitochondrial diseases can be inherited from either the mother's or father's side, or they can occur spontaneously due to genetic mutations. They can range from mild to severe and can even be life-threatening in some cases.

Motor neurons are specialized nerve cells in the brain and spinal cord that play a crucial role in controlling voluntary muscle movements. They transmit electrical signals from the brain to the muscles, enabling us to perform actions such as walking, talking, and swallowing. There are two types of motor neurons: upper motor neurons, which originate in the brain's motor cortex and travel down to the brainstem and spinal cord; and lower motor neurons, which extend from the brainstem and spinal cord to the muscles. Damage or degeneration of these motor neurons can lead to various neurological disorders, such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA).

Ubiquitin is a small protein that is present in all eukaryotic cells and plays a crucial role in the regulation of various cellular processes, such as protein degradation, DNA repair, and stress response. It is involved in marking proteins for destruction by attaching to them, a process known as ubiquitination. This modification can target proteins for degradation by the proteasome, a large protein complex that breaks down unneeded or damaged proteins in the cell. Ubiquitin also has other functions, such as regulating the localization and activity of certain proteins. The ability of ubiquitin to modify many different proteins and play a role in multiple cellular processes makes it an essential player in maintaining cellular homeostasis.

Central nervous system (CNS) diseases refer to medical conditions that primarily affect the brain and spinal cord. The CNS is responsible for controlling various functions in the body, including movement, sensation, cognition, and behavior. Therefore, diseases of the CNS can have significant impacts on a person's quality of life and overall health.

There are many different types of CNS diseases, including:

1. Infectious diseases: These are caused by viruses, bacteria, fungi, or parasites that infect the brain or spinal cord. Examples include meningitis, encephalitis, and polio.
2. Neurodegenerative diseases: These are characterized by progressive loss of nerve cells in the brain or spinal cord. Examples include Alzheimer's disease, Parkinson's disease, and Huntington's disease.
3. Structural diseases: These involve damage to the physical structure of the brain or spinal cord, such as from trauma, tumors, or stroke.
4. Functional diseases: These affect the function of the nervous system without obvious structural damage, such as multiple sclerosis and epilepsy.
5. Genetic disorders: Some CNS diseases are caused by genetic mutations, such as spinal muscular atrophy and Friedreich's ataxia.

Symptoms of CNS diseases can vary widely depending on the specific condition and the area of the brain or spinal cord that is affected. They may include muscle weakness, paralysis, seizures, loss of sensation, difficulty with coordination and balance, confusion, memory loss, changes in behavior or mood, and pain. Treatment for CNS diseases depends on the specific condition and may involve medications, surgery, rehabilitation therapy, or a combination of these approaches.

The hippocampus is a complex, curved formation in the brain that resembles a seahorse (hence its name, from the Greek word "hippos" meaning horse and "kampos" meaning sea monster). It's part of the limbic system and plays crucial roles in the formation of memories, particularly long-term ones.

This region is involved in spatial navigation and cognitive maps, allowing us to recognize locations and remember how to get to them. Additionally, it's one of the first areas affected by Alzheimer's disease, which often results in memory loss as an early symptom.

Anatomically, it consists of two main parts: the Ammon's horn (or cornu ammonis) and the dentate gyrus. These structures are made up of distinct types of neurons that contribute to different aspects of learning and memory.

I'm not aware of a medical definition for the term "Cycas." It is a genus name in botany, referring to a group of plants commonly known as cycads. Cycads are ancient seed plants that have been on Earth for millions of years. They are often grown as ornamental plants due to their unique appearance.

While there may not be a direct medical definition for "Cycas," it is worth noting that some parts of the cycad plant, particularly the seeds, contain toxic compounds that can cause serious health issues in both humans and animals if ingested. These toxins can affect the nervous system, liver, and kidneys, leading to symptoms such as vomiting, seizures, and even death in severe cases.

Therefore, while "Cycas" may not have a medical definition per se, it is still important to be aware of its potential health risks.

Iron-binding proteins, also known as transferrins, are a type of protein responsible for the transport and storage of iron in the body. They play a crucial role in maintaining iron homeostasis by binding free iron ions and preventing them from participating in harmful chemical reactions that can produce reactive oxygen species (ROS) and cause cellular damage.

Transferrin is the primary iron-binding protein found in blood plasma, while lactoferrin is found in various exocrine secretions such as milk, tears, and saliva. Both transferrin and lactoferrin have a similar structure, consisting of two lobes that can bind one ferric ion (Fe3+) each. When iron is bound to these proteins, they are called holo-transferrin or holo-lactoferrin; when they are unbound, they are referred to as apo-transferrin or apo-lactoferrin.

Iron-binding proteins have a high affinity for iron and can regulate the amount of free iron available in the body. They help prevent iron overload, which can lead to oxidative stress and cellular damage, as well as iron deficiency, which can result in anemia and other health problems.

In summary, iron-binding proteins are essential for maintaining iron homeostasis by transporting and storing iron ions, preventing them from causing harm to the body's cells.

The proteasome endopeptidase complex is a large protein complex found in the cells of eukaryotic organisms, as well as in archaea and some bacteria. It plays a crucial role in the degradation of damaged or unneeded proteins through a process called proteolysis. The proteasome complex contains multiple subunits, including both regulatory and catalytic particles.

The catalytic core of the proteasome is composed of four stacked rings, each containing seven subunits, forming a structure known as the 20S core particle. Three of these rings are made up of beta-subunits that contain the proteolytic active sites, while the fourth ring consists of alpha-subunits that control access to the interior of the complex.

The regulatory particles, called 19S or 11S regulators, cap the ends of the 20S core particle and are responsible for recognizing, unfolding, and translocating targeted proteins into the catalytic chamber. The proteasome endopeptidase complex can cleave peptide bonds in various ways, including hydrolysis of ubiquitinated proteins, which is an essential mechanism for maintaining protein quality control and regulating numerous cellular processes, such as cell cycle progression, signal transduction, and stress response.

In summary, the proteasome endopeptidase complex is a crucial intracellular machinery responsible for targeted protein degradation through proteolysis, contributing to various essential regulatory functions in cells.

Spinal muscular atrophy (SMA) is a genetic disorder that affects the motor neurons in the spinal cord, leading to muscle weakness and atrophy. It is caused by a mutation in the survival motor neuron 1 (SMN1) gene, which results in a deficiency of SMN protein necessary for the survival of motor neurons.

There are several types of SMA, classified based on the age of onset and severity of symptoms. The most common type is type 1, also known as Werdnig-Hoffmann disease, which presents in infancy and is characterized by severe muscle weakness, hypotonia, and feeding difficulties. Other types include type 2 (intermediate SMA), type 3 (Kugelberg-Welander disease), and type 4 (adult-onset SMA).

The symptoms of SMA may include muscle wasting, fasciculations, weakness, hypotonia, respiratory difficulties, and mobility impairment. The diagnosis of SMA typically involves genetic testing to confirm the presence of a mutation in the SMN1 gene. Treatment options for SMA may include medications, physical therapy, assistive devices, and respiratory support.

The cerebral cortex is the outermost layer of the brain, characterized by its intricate folded structure and wrinkled appearance. It is a region of great importance as it plays a key role in higher cognitive functions such as perception, consciousness, thought, memory, language, and attention. The cerebral cortex is divided into two hemispheres, each containing four lobes: the frontal, parietal, temporal, and occipital lobes. These areas are responsible for different functions, with some regions specializing in sensory processing while others are involved in motor control or associative functions. The cerebral cortex is composed of gray matter, which contains neuronal cell bodies, and is covered by a layer of white matter that consists mainly of myelinated nerve fibers.

Pick's disease, also known as Frontotemporal dementia (FTD), is a rare form of degenerative brain disorder that affects the frontal and temporal lobes of the brain. It is characterized by progressive shrinkage (atrophy) of these regions, resulting in a decline in cognitive abilities, behavioral changes, and language difficulties.

The medical definition of Pick's disease includes the following key features:

1. Progressive deterioration of cognitive functions, including memory, judgment, and problem-solving skills.
2. Changes in personality, emotional blunting, and loss of social inhibitions.
3. Language difficulties, such as difficulty with word finding, grammar, and comprehension.
4. Presence of abnormal protein deposits called Pick bodies or Pick cells in the affected brain regions.
5. Exclusion of other causes of dementia, such as Alzheimer's disease, vascular dementia, or Lewy body dementia.

Pick's disease typically affects people between the ages of 40 and 60, and it tends to progress more rapidly than other forms of dementia. Currently, there is no cure for Pick's disease, and treatment focuses on managing symptoms and improving quality of life.

Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.

The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.

Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.

Cell survival refers to the ability of a cell to continue living and functioning normally, despite being exposed to potentially harmful conditions or treatments. This can include exposure to toxins, radiation, chemotherapeutic drugs, or other stressors that can damage cells or interfere with their normal processes.

In scientific research, measures of cell survival are often used to evaluate the effectiveness of various therapies or treatments. For example, researchers may expose cells to a particular drug or treatment and then measure the percentage of cells that survive to assess its potential therapeutic value. Similarly, in toxicology studies, measures of cell survival can help to determine the safety of various chemicals or substances.

It's important to note that cell survival is not the same as cell proliferation, which refers to the ability of cells to divide and multiply. While some treatments may promote cell survival, they may also inhibit cell proliferation, making them useful for treating diseases such as cancer. Conversely, other treatments may be designed to specifically target and kill cancer cells, even if it means sacrificing some healthy cells in the process.

FUS (Fused in Sarcoma) is a protein that in humans is encoded by the FUS gene. It is primarily located in the nucleus of the cell, but can also be found in the cytoplasm. FUS belongs to the family of RNA-binding proteins, which means it has the ability to bind to RNA molecules and play a role in post-transcriptional regulation of gene expression.

FUS has several functions, including:

1. Transcriptional regulation: FUS can interact with transcription factors and modulate the transcription of genes.
2. mRNA processing: FUS is involved in various aspects of mRNA processing, such as splicing, transport, localization, and stability.
3. DNA repair: FUS plays a role in DNA damage response and repair mechanisms.
4. Translational regulation: FUS can also regulate translation by interacting with ribosomes and other translational factors.

Mutations in the FUS gene have been associated with several neurodegenerative disorders, such as amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). These mutations often lead to an abnormal cytoplasmic accumulation of FUS protein, which can form aggregates and contribute to the pathogenesis of these diseases.

Neuroglia, also known as glial cells or simply glia, are non-neuronal cells that provide support and protection for neurons in the nervous system. They maintain homeostasis, form myelin sheaths around nerve fibers, and provide structural support. They also play a role in the immune response of the central nervous system. Some types of neuroglia include astrocytes, oligodendrocytes, microglia, and ependymal cells.

Gliosis is a term used in histopathology and neuroscience to describe the reaction of support cells in the brain, called glial cells, to injury or disease. This response includes an increase in the number and size of glial cells, as well as changes in their shape and function. The most common types of glial cells involved in gliosis are astrocytes and microglia.

Gliosis can be triggered by a variety of factors, including trauma, infection, inflammation, neurodegenerative diseases, and stroke. In response to injury or disease, astrocytes become hypertrophied (enlarged) and undergo changes in their gene expression profile that can lead to the production of various proteins, such as glial fibrillary acidic protein (GFAP). These changes can result in the formation of a dense network of astrocytic processes, which can contribute to the formation of a glial scar.

Microglia, another type of glial cell, become activated during gliosis and play a role in the immune response in the central nervous system (CNS). They can release pro-inflammatory cytokines, chemokines, and reactive oxygen species that contribute to the inflammatory response.

While gliosis is a protective response aimed at containing damage and promoting tissue repair, it can also have negative consequences. For example, the formation of glial scars can impede axonal regeneration and contribute to neurological deficits. Additionally, chronic activation of microglia has been implicated in various neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

'Gene expression regulation' refers to the processes that control whether, when, and where a particular gene is expressed, meaning the production of a specific protein or functional RNA encoded by that gene. This complex mechanism can be influenced by various factors such as transcription factors, chromatin remodeling, DNA methylation, non-coding RNAs, and post-transcriptional modifications, among others. Proper regulation of gene expression is crucial for normal cellular function, development, and maintaining homeostasis in living organisms. Dysregulation of gene expression can lead to various diseases, including cancer and genetic disorders.

Nervous system diseases, also known as neurological disorders, refer to a group of conditions that affect the nervous system, which includes the brain, spinal cord, nerves, and muscles. These diseases can affect various functions of the body, such as movement, sensation, cognition, and behavior. They can be caused by genetics, infections, injuries, degeneration, or tumors. Examples of nervous system diseases include Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, migraine, stroke, and neuroinfections like meningitis and encephalitis. The symptoms and severity of these disorders can vary widely, ranging from mild to severe and debilitating.

Amyloid plaque is a pathological hallmark of several degenerative diseases, including Alzheimer's disease. It refers to extracellular deposits of misfolded proteins that accumulate in various tissues and organs, but are most commonly found in the brain. The main component of these plaques is an abnormally folded form of a protein called amyloid-beta (Aβ). This protein is produced through the normal processing of the amyloid precursor protein (APP), but in amyloid plaques, it aggregates into insoluble fibrils that form the core of the plaque.

The accumulation of amyloid plaques is thought to contribute to neurodegeneration and cognitive decline in Alzheimer's disease and other related disorders. The exact mechanisms by which this occurs are not fully understood, but it is believed that the aggregation of Aβ into plaques leads to the disruption of neuronal function and viability, as well as the activation of inflammatory responses that can further damage brain tissue.

It's important to note that while amyloid plaques are a key feature of Alzheimer's disease, they are not exclusive to this condition. Amyloid plaques have also been found in other neurodegenerative disorders, as well as in some normal aging brains, although their significance in these contexts is less clear.

Reactive Oxygen Species (ROS) are highly reactive molecules containing oxygen, including peroxides, superoxide, hydroxyl radical, and singlet oxygen. They are naturally produced as byproducts of normal cellular metabolism in the mitochondria, and can also be generated by external sources such as ionizing radiation, tobacco smoke, and air pollutants. At low or moderate concentrations, ROS play important roles in cell signaling and homeostasis, but at high concentrations, they can cause significant damage to cell structures, including lipids, proteins, and DNA, leading to oxidative stress and potential cell death.

Multiple System Atrophy (MSA) is a rare, progressive neurodegenerative disorder that affects multiple systems in the body. It is characterized by a combination of symptoms including Parkinsonism (such as stiffness, slowness of movement, and tremors), cerebellar ataxia (lack of muscle coordination), autonomic dysfunction (problems with the autonomic nervous system which controls involuntary actions like heart rate, blood pressure, sweating, and digestion), and pyramidal signs (abnormalities in the corticospinal tracts that control voluntary movements).

The disorder is caused by the degeneration of nerve cells in various parts of the brain and spinal cord, leading to a loss of function in these areas. The exact cause of MSA is unknown, but it is thought to involve a combination of genetic and environmental factors. There is currently no cure for MSA, and treatment is focused on managing symptoms and improving quality of life.

Nuclear proteins are a category of proteins that are primarily found in the nucleus of a eukaryotic cell. They play crucial roles in various nuclear functions, such as DNA replication, transcription, repair, and RNA processing. This group includes structural proteins like lamins, which form the nuclear lamina, and regulatory proteins, such as histones and transcription factors, that are involved in gene expression. Nuclear localization signals (NLS) often help target these proteins to the nucleus by interacting with importin proteins during active transport across the nuclear membrane.

Genetically modified animals (GMAs) are those whose genetic makeup has been altered using biotechnological techniques. This is typically done by introducing one or more genes from another species into the animal's genome, resulting in a new trait or characteristic that does not naturally occur in that species. The introduced gene is often referred to as a transgene.

The process of creating GMAs involves several steps:

1. Isolation: The desired gene is isolated from the DNA of another organism.
2. Transfer: The isolated gene is transferred into the target animal's cells, usually using a vector such as a virus or bacterium.
3. Integration: The transgene integrates into the animal's chromosome, becoming a permanent part of its genetic makeup.
4. Selection: The modified cells are allowed to multiply, and those that contain the transgene are selected for further growth and development.
5. Breeding: The genetically modified individuals are bred to produce offspring that carry the desired trait.

GMAs have various applications in research, agriculture, and medicine. In research, they can serve as models for studying human diseases or testing new therapies. In agriculture, GMAs can be developed to exhibit enhanced growth rates, improved disease resistance, or increased nutritional value. In medicine, GMAs may be used to produce pharmaceuticals or other therapeutic agents within their bodies.

Examples of genetically modified animals include mice with added genes for specific proteins that make them useful models for studying human diseases, goats that produce a human protein in their milk to treat hemophilia, and pigs with enhanced resistance to certain viruses that could potentially be used as organ donors for humans.

It is important to note that the use of genetically modified animals raises ethical concerns related to animal welfare, environmental impact, and potential risks to human health. These issues must be carefully considered and addressed when developing and implementing GMA technologies.

The Substantia Nigra is a region in the midbrain that plays a crucial role in movement control and reward processing. It is composed of two parts: the pars compacta and the pars reticulata. The pars compacta contains dopamine-producing neurons, whose loss or degeneration is associated with Parkinson's disease, leading to motor symptoms such as tremors, rigidity, and bradykinesia.

In summary, Substantia Nigra is a brain structure that contains dopamine-producing cells and is involved in movement control and reward processing. Its dysfunction or degeneration can lead to neurological disorders like Parkinson's disease.

Molecular chaperones are a group of proteins that assist in the proper folding and assembly of other protein molecules, helping them achieve their native conformation. They play a crucial role in preventing protein misfolding and aggregation, which can lead to the formation of toxic species associated with various neurodegenerative diseases. Molecular chaperones are also involved in protein transport across membranes, degradation of misfolded proteins, and protection of cells under stress conditions. Their function is generally non-catalytic and ATP-dependent, and they often interact with their client proteins in a transient manner.

PrP^Sc (prion protein scrapie) is a misfolded, abnormal conformational isoform of the prion protein (PrP), which is associated with a group of progressive neurodegenerative disorders known as transmissible spongiform encephalopathies (TSEs). These diseases affect both humans and animals and include conditions like bovine spongiform encephalopathy (BSE or "mad cow disease") in cattle, scrapie in sheep, and variant Creutzfeldt-Jakob disease (vCJD) in humans.

The PrP protein is a naturally occurring, normal cellular protein found primarily in the brain and central nervous system. It has a predominantly alpha-helical structure under physiological conditions. However, during the development of prion diseases, PrP^Sc forms through a conformational change where the alpha-helical regions are replaced by beta-sheet structures. This misfolded protein can aggregate and form amyloid fibrils, which deposit in various brain regions leading to neurodegeneration, spongiform changes, gliosis, and neuronal loss.

Importantly, PrP^Sc is thought to have self-propagating properties, as it can induce the conversion of normal PrP into more PrP^Sc through a process called seeded polymerization or templated misfolding. This mechanism is believed to underlie the infectious nature and transmissibility of prion diseases.

Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.

Beta-synuclein is a protein that is encoded by the SNCB gene in humans. It is a member of the synuclein family, which also includes alpha-synuclein and gamma-synuclein. Beta-synuclein is primarily found in the brain and is expressed at high levels in neurons.

Like alpha-synuclein, beta-synuclein has been shown to interact with lipids and play a role in the maintenance of synaptic function. However, unlike alpha-synuclein, which can form aggregates that are associated with neurodegenerative diseases such as Parkinson's disease and dementia with Lewy bodies, beta-synuclein does not appear to form aggregates under normal physiological conditions.

Some studies have suggested that beta-synuclein may play a protective role in the brain by inhibiting the aggregation of alpha-synuclein. However, other studies have suggested that beta-synuclein may contribute to neurodegeneration in certain contexts, such as in the presence of mutations or under conditions of cellular stress.

Overall, while the exact functions and regulatory mechanisms of beta-synuclein are still being elucidated, it is clear that this protein plays important roles in neuronal function and may have implications for neurodegenerative diseases.

The Rotarod performance test is not a medical diagnosis or condition, but rather a laboratory test used in both preclinical research and clinical settings to evaluate various aspects of motor function and balance in animals, including mice and rats. The test is often used to assess the neurological status, sensorimotor function, and coordination abilities of animals following drug treatments, surgical interventions, or in models of neurodegenerative diseases.

In this test, a rodent is placed on a rotating rod with a diameter that allows the animal to comfortably grip it. The rotation speed gradually increases over time, and the researcher records how long the animal can maintain its balance and stay on the rod without falling off. This duration is referred to as the "latency to fall" or "rotarod performance."

The Rotarod performance test offers several advantages, such as its sensitivity to various neurological impairments, ease of use, and ability to provide quantitative data for statistical analysis. It can help researchers evaluate potential therapeutic interventions, monitor disease progression, and investigate the underlying mechanisms of motor function and balance in health and disease.

Diamino acids are a type of modified amino acids that contain two amino groups (-NH2) in their side chain. In regular amino acids, the side chain is composed of a specific arrangement of carbon, hydrogen, oxygen, and sometimes sulfur atoms. However, in diamino acids, one or both of the hydrogen atoms attached to the central carbon atom (alpha carbon) are replaced by amino groups.

There are two types of diamino acids: symmetric and asymmetric. Symmetric diamino acids have identical side chains on both sides of the alpha carbon atom, while asymmetric diamino acids have different side chains on each side.

Diamino acids play a crucial role in various biological processes, such as protein synthesis, cell signaling, and neurotransmission. They can be found naturally in some proteins or can be synthesized artificially for use in research and medical applications.

It is important to note that diamino acids are not one of the twenty standard amino acids that make up proteins. Instead, they are considered non-proteinogenic amino acids, which means they are not typically encoded by DNA and are not directly involved in protein synthesis. However, some modified forms of diamino acids can be found in certain proteins as a result of post-translational modifications.

Secondary Parkinson's disease, also known as acquired or symptomatic Parkinsonism, is a clinical syndrome characterized by the signs and symptoms of classic Parkinson's disease (tremor at rest, rigidity, bradykinesia, and postural instability) but caused by a known secondary cause. These causes can include various conditions such as brain injuries, infections, drugs or toxins, metabolic disorders, and vascular damage. The underlying pathology of secondary Parkinson's disease is different from that of classic Parkinson's disease, which is primarily due to the degeneration of dopamine-producing neurons in a specific area of the brain called the substantia nigra pars compacta.

An axon is a long, slender extension of a neuron (a type of nerve cell) that conducts electrical impulses (nerve impulses) away from the cell body to target cells, such as other neurons or muscle cells. Axons can vary in length from a few micrometers to over a meter long and are typically surrounded by a myelin sheath, which helps to insulate and protect the axon and allows for faster transmission of nerve impulses.

Axons play a critical role in the functioning of the nervous system, as they provide the means by which neurons communicate with one another and with other cells in the body. Damage to axons can result in serious neurological problems, such as those seen in spinal cord injuries or neurodegenerative diseases like multiple sclerosis.

Intranuclear inclusion bodies are abnormal, rounded structures found within the nucleus of a cell. They are composed of aggregated proteins or other cellular components and can be associated with various viral infections and certain genetic disorders. These inclusion bodies can interfere with normal nuclear functions, leading to cell damage and contributing to the pathogenesis of diseases such as cytomegalovirus infection, rabies, and some forms of neurodegenerative disorders like polyglutamine diseases. The presence of intranuclear inclusion bodies is often used in diagnostic pathology to help identify specific underlying conditions.

DNA repeat expansion is a genetic alteration in which a particular sequence of DNA base pairs is repeated multiple times. In normal genes, these repeats are relatively short and stable, but in certain diseases, the number of repeats can expand beyond a threshold, leading to changes in the structure or function of the gene. This type of mutation is often associated with neurological and neuromuscular disorders, such as Huntington's disease, myotonic dystrophy, and fragile X syndrome. The expanded repeats can also be unstable and may increase in size over generations, leading to more severe symptoms or earlier age of onset.

The spinal cord is a major part of the nervous system, extending from the brainstem and continuing down to the lower back. It is a slender, tubular bundle of nerve fibers (axons) and support cells (glial cells) that carries signals between the brain and the rest of the body. The spinal cord primarily serves as a conduit for motor information, which travels from the brain to the muscles, and sensory information, which travels from the body to the brain. It also contains neurons that can independently process and respond to information within the spinal cord without direct input from the brain.

The spinal cord is protected by the bony vertebral column (spine) and is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each segment corresponds to a specific region of the body and gives rise to pairs of spinal nerves that exit through the intervertebral foramina at each level.

The spinal cord is responsible for several vital functions, including:

1. Reflexes: Simple reflex actions, such as the withdrawal reflex when touching a hot surface, are mediated by the spinal cord without involving the brain.
2. Muscle control: The spinal cord carries motor signals from the brain to the muscles, enabling voluntary movement and muscle tone regulation.
3. Sensory perception: The spinal cord transmits sensory information, such as touch, temperature, pain, and vibration, from the body to the brain for processing and awareness.
4. Autonomic functions: The sympathetic and parasympathetic divisions of the autonomic nervous system originate in the thoracolumbar and sacral regions of the spinal cord, respectively, controlling involuntary physiological responses like heart rate, blood pressure, digestion, and respiration.

Damage to the spinal cord can result in various degrees of paralysis or loss of sensation below the level of injury, depending on the severity and location of the damage.

Dopaminergic neurons are a type of specialized brain cells that produce, synthesize, and release the neurotransmitter dopamine. These neurons play crucial roles in various brain functions, including motivation, reward processing, motor control, and cognition. They are primarily located in several regions of the midbrain, such as the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA).

Dopaminergic neurons have a unique physiology characterized by their ability to generate slow, irregular electrical signals called pacemaker activity. This distinctive firing pattern allows dopamine to be released in a controlled manner, which is essential for proper brain function.

The degeneration and loss of dopaminergic neurons in the SNc are associated with Parkinson's disease, a neurodegenerative disorder characterized by motor impairments such as tremors, rigidity, and bradykinesia (slowness of movement). The reduction in dopamine levels caused by this degeneration leads to an imbalance in the brain's neural circuitry, resulting in the characteristic symptoms of Parkinson's disease.

Atrophy is a medical term that refers to the decrease in size and wasting of an organ or tissue due to the disappearance of cells, shrinkage of cells, or decreased number of cells. This process can be caused by various factors such as disuse, aging, degeneration, injury, or disease.

For example, if a muscle is immobilized for an extended period, it may undergo atrophy due to lack of use. Similarly, certain medical conditions like diabetes, cancer, and heart failure can lead to the wasting away of various tissues and organs in the body.

Atrophy can also occur as a result of natural aging processes, leading to decreased muscle mass and strength in older adults. In general, atrophy is characterized by a decrease in the volume or weight of an organ or tissue, which can have significant impacts on its function and overall health.

Western blotting is a laboratory technique used in molecular biology to detect and quantify specific proteins in a mixture of many different proteins. This technique is commonly used to confirm the expression of a protein of interest, determine its size, and investigate its post-translational modifications. The name "Western" blotting distinguishes this technique from Southern blotting (for DNA) and Northern blotting (for RNA).

The Western blotting procedure involves several steps:

1. Protein extraction: The sample containing the proteins of interest is first extracted, often by breaking open cells or tissues and using a buffer to extract the proteins.
2. Separation of proteins by electrophoresis: The extracted proteins are then separated based on their size by loading them onto a polyacrylamide gel and running an electric current through the gel (a process called sodium dodecyl sulfate-polyacrylamide gel electrophoresis or SDS-PAGE). This separates the proteins according to their molecular weight, with smaller proteins migrating faster than larger ones.
3. Transfer of proteins to a membrane: After separation, the proteins are transferred from the gel onto a nitrocellulose or polyvinylidene fluoride (PVDF) membrane using an electric current in a process called blotting. This creates a replica of the protein pattern on the gel but now immobilized on the membrane for further analysis.
4. Blocking: The membrane is then blocked with a blocking agent, such as non-fat dry milk or bovine serum albumin (BSA), to prevent non-specific binding of antibodies in subsequent steps.
5. Primary antibody incubation: A primary antibody that specifically recognizes the protein of interest is added and allowed to bind to its target protein on the membrane. This step may be performed at room temperature or 4°C overnight, depending on the antibody's properties.
6. Washing: The membrane is washed with a buffer to remove unbound primary antibodies.
7. Secondary antibody incubation: A secondary antibody that recognizes the primary antibody (often coupled to an enzyme or fluorophore) is added and allowed to bind to the primary antibody. This step may involve using a horseradish peroxidase (HRP)-conjugated or alkaline phosphatase (AP)-conjugated secondary antibody, depending on the detection method used later.
8. Washing: The membrane is washed again to remove unbound secondary antibodies.
9. Detection: A detection reagent is added to visualize the protein of interest by detecting the signal generated from the enzyme-conjugated or fluorophore-conjugated secondary antibody. This can be done using chemiluminescent, colorimetric, or fluorescent methods.
10. Analysis: The resulting image is analyzed to determine the presence and quantity of the protein of interest in the sample.

Western blotting is a powerful technique for identifying and quantifying specific proteins within complex mixtures. It can be used to study protein expression, post-translational modifications, protein-protein interactions, and more. However, it requires careful optimization and validation to ensure accurate and reproducible results.

The corpus striatum is a part of the brain that plays a crucial role in movement, learning, and cognition. It consists of two structures called the caudate nucleus and the putamen, which are surrounded by the external and internal segments of the globus pallidus. Together, these structures form the basal ganglia, a group of interconnected neurons that help regulate voluntary movement.

The corpus striatum receives input from various parts of the brain, including the cerebral cortex, thalamus, and other brainstem nuclei. It processes this information and sends output to the globus pallidus and substantia nigra, which then project to the thalamus and back to the cerebral cortex. This feedback loop helps coordinate and fine-tune movements, allowing for smooth and coordinated actions.

Damage to the corpus striatum can result in movement disorders such as Parkinson's disease, Huntington's disease, and dystonia. These conditions are characterized by abnormal involuntary movements, muscle stiffness, and difficulty initiating or controlling voluntary movements.

TDP-43 proteinopathies refer to a group of neurodegenerative disorders characterized by the abnormal accumulation and aggregation of the TAR DNA-binding protein 43 (TDP-43) in neuronal and glial cells. The accumulated TDP-43 forms inclusions that are rich in ubiquitin and are a hallmark of these disorders.

TDP-43 is a nuclear protein involved in various cellular processes, including transcription, splicing, and transport of RNA. In TDP-43 proteinopathies, the protein undergoes post-translational modifications that lead to its mislocalization from the nucleus to the cytoplasm, where it forms aggregates.

TDP-43 proteinopathies include several neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration (FTLD), and Alzheimer's disease (AD). In ALS, TDP-43 pathology is present in almost all cases, while in FTLD, it is found in about half of the cases. In AD, TDP-43 pathology is less common but still significant, particularly in patients with coexisting dementia.

TDP-43 proteinopathies are associated with various clinical manifestations depending on the specific disorder and the extent and location of TDP-43 aggregation. These manifestations include motor neuron degeneration, cognitive decline, behavioral changes, and language impairments. The underlying mechanisms leading to TDP-43 mislocalization and aggregation are not fully understood but are thought to involve genetic, environmental, and aging factors.

Antioxidants are substances that can prevent or slow damage to cells caused by free radicals, which are unstable molecules that the body produces as a reaction to environmental and other pressures. Antioxidants are able to neutralize free radicals by donating an electron to them, thus stabilizing them and preventing them from causing further damage to the cells.

Antioxidants can be found in a variety of foods, including fruits, vegetables, nuts, and grains. Some common antioxidants include vitamins C and E, beta-carotene, and selenium. Antioxidants are also available as dietary supplements.

In addition to their role in protecting cells from damage, antioxidants have been studied for their potential to prevent or treat a number of health conditions, including cancer, heart disease, and age-related macular degeneration. However, more research is needed to fully understand the potential benefits and risks of using antioxidant supplements.

Cyclin-Dependent Kinase 5 (CDK5) is a type of protein kinase that plays crucial roles in the regulation of various cellular processes, particularly in neurons. Unlike other cyclin-dependent kinases, CDK5 is activated by associating with regulatory subunits called cyclins, specifically cyclin I and cyclin D1, but not during the cell cycle.

CDK5 activity is primarily involved in the development and functioning of the nervous system, where it regulates neuronal migration, differentiation, and synaptic plasticity. It has been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, and various neurodevelopmental conditions.

CDK5 activity is tightly regulated by phosphorylation and interacting partners. Dysregulation of CDK5 can lead to abnormal neuronal function and contribute to the pathogenesis of neurological disorders.

A phenotype is the physical or biochemical expression of an organism's genes, or the observable traits and characteristics resulting from the interaction of its genetic constitution (genotype) with environmental factors. These characteristics can include appearance, development, behavior, and resistance to disease, among others. Phenotypes can vary widely, even among individuals with identical genotypes, due to differences in environmental influences, gene expression, and genetic interactions.

Neurofilament proteins (NFs) are type IV intermediate filament proteins that are specific to neurons. They are the major structural components of the neuronal cytoskeleton and play crucial roles in maintaining the structural integrity, stability, and diameter of axons. Neurofilaments are composed of three subunits: light (NFL), medium (NFM), and heavy (NFH) neurofilament proteins, which differ in their molecular weights. These subunits assemble into heteropolymers to form the neurofilament core, while the C-terminal tails of NFH and NFM extend outward from the core, interacting with other cellular components and participating in various neuronal functions. Increased levels of neurofilament proteins, particularly NFL, in cerebrospinal fluid (CSF) and blood are considered biomarkers for axonal damage and neurodegeneration in several neurological disorders, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

The Amyloid Beta-Protein Precursor (AβPP) is a type of transmembrane protein that is widely expressed in various tissues and organs, including the brain. It plays a crucial role in normal physiological processes, such as neuronal development, synaptic plasticity, and repair.

AβPP undergoes proteolytic processing by enzymes called secretases, resulting in the production of several protein fragments, including the amyloid-beta (Aβ) peptide. Aβ is a small peptide that can aggregate and form insoluble fibrils, which are the main component of amyloid plaques found in the brains of patients with Alzheimer's disease (AD).

The accumulation of Aβ plaques is believed to contribute to the neurodegeneration and cognitive decline observed in AD. Therefore, AβPP and its proteolytic processing have been the focus of extensive research aimed at understanding the pathogenesis of AD and developing potential therapies.

Neuroaxonal dystrophies (NADs) are a group of inherited neurological disorders characterized by degeneration of the neuronal axons, which are the long extensions of nerve cells that transmit impulses to other cells. This degeneration leads to progressive loss of motor and cognitive functions.

The term "neuroaxonal dystrophy" refers to a specific pattern of abnormalities seen on electron microscopy in nerve cells, including accumulation of membranous structures called "spheroids" or "tubulovesicular structures" within the axons.

NADs can be caused by mutations in various genes that play a role in maintaining the structure and function of neuronal axons. The most common forms of NADs include Infantile Neuroaxonal Dystrophy (INAD) or Seitelberger's Disease, and Late-Onset Neuroaxonal Dystrophy (LONAD).

Symptoms of INAD typically begin between ages 6 months and 2 years, and may include muscle weakness, hypotonia, decreased reflexes, vision loss, hearing impairment, and developmental delay. LONAD usually presents in childhood or adolescence with symptoms such as ataxia, dysarthria, cognitive decline, and behavioral changes.

Currently, there is no cure for NADs, and treatment is focused on managing symptoms and improving quality of life.

Ataxia is a medical term that refers to a group of disorders affecting coordination, balance, and speech. It is characterized by a lack of muscle control during voluntary movements, causing unsteady or awkward movements, and often accompanied by tremors. Ataxia can affect various parts of the body, such as the limbs, trunk, eyes, and speech muscles. The condition can be congenital or acquired, and it can result from damage to the cerebellum, spinal cord, or sensory nerves. There are several types of ataxia, including hereditary ataxias, degenerative ataxias, cerebellar ataxias, and acquired ataxias, each with its own specific causes, symptoms, and prognosis. Treatment for ataxia typically focuses on managing symptoms and improving quality of life, as there is no cure for most forms of the disorder.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Encephalitis is defined as inflammation of the brain parenchyma, which is often caused by viral infections but can also be due to bacterial, fungal, or parasitic infections, autoimmune disorders, or exposure to toxins. The infection or inflammation can cause various symptoms such as headache, fever, confusion, seizures, and altered consciousness, ranging from mild symptoms to severe cases that can lead to brain damage, long-term disabilities, or even death.

The diagnosis of encephalitis typically involves a combination of clinical evaluation, imaging studies (such as MRI or CT scans), and laboratory tests (such as cerebrospinal fluid analysis). Treatment may include antiviral medications, corticosteroids, immunoglobulins, and supportive care to manage symptoms and prevent complications.

PrPc proteins, also known as cellular prion proteins, are a type of protein found on the surface of many types of cells in the body, including neurons in the brain. The normal function of PrPc proteins is not entirely clear, but they are believed to play a role in various physiological processes such as protecting nerve cells from damage, regulating metal ion homeostasis, and participating in cell signaling pathways.

PrPc proteins are composed of 253 amino acids and have a molecular weight of approximately 35 kDa. They contain a highly conserved domain called the prion protein domain (PRD), which is rich in alpha-helices and contains a copper-binding site. The PRD is necessary for the normal function of PrPc proteins, but it is also the region that undergoes conformational changes to form the abnormal, disease-associated form of the protein called PrPSc.

PrPSc proteins are misfolded and aggregated forms of PrPc proteins that are associated with a group of neurodegenerative diseases known as transmissible spongiform encephalopathies (TSEs), including bovine spongiform encephalopathy (BSE or "mad cow disease"), scrapie in sheep, and variant Creutzfeldt-Jakob disease (vCJD) in humans. The misfolded PrPSc proteins can cause other normal PrPc proteins to also misfold and aggregate, leading to the formation of amyloid fibrils that accumulate in the brain and cause neurodegeneration.

Nervous system trauma, also known as neurotrauma, refers to damage or injury to the nervous system, including the brain and spinal cord. This type of trauma can result from various causes, such as vehicular accidents, sports injuries, falls, violence, or penetrating traumas. Nervous system trauma can lead to temporary or permanent impairments in sensory, motor, or cognitive functions, depending on the severity and location of the injury.

Traumatic brain injury (TBI) is a common form of nervous system trauma that occurs when an external force causes brain dysfunction. TBIs can be classified as mild, moderate, or severe, based on factors such as loss of consciousness, memory loss, and neurological deficits. Mild TBIs, also known as concussions, may not cause long-term damage but still require medical attention to ensure proper healing and prevent further complications.

Spinal cord injuries (SCI) are another form of nervous system trauma that can have severe consequences. SCI occurs when the spinal cord is damaged due to a sudden, traumatic blow or cut, causing loss of motor function, sensation, or autonomic function below the level of injury. The severity and location of the injury determine the extent of impairment, which can range from partial to complete paralysis.

Immediate medical intervention is crucial in cases of nervous system trauma to minimize secondary damage, prevent complications, and optimize recovery outcomes. Treatment options may include surgery, medication, rehabilitation, or a combination of these approaches.

Creutzfeldt-Jakob syndrome (CJD) is a rare, degenerative, and fatal brain disorder. It is caused by an abnormal form of protein called prion that can cause normal proteins in the brain to fold into abnormal shapes and accumulate, leading to damage and death of brain cells.

The symptoms of CJD usually develop over a period of several months and include rapidly progressing dementia, memory loss, confusion, coordination problems, muscle stiffness, twitching, and shaking. Some people may also experience visual hallucinations, changes in personality, or depression.

There are three main types of CJD: sporadic, inherited, and acquired. Sporadic CJD is the most common form and accounts for about 85% of all cases. It occurs spontaneously with no known cause. Inherited CJD is caused by a genetic mutation that is passed down from parents to their children. Acquired CJD is caused by exposure to contaminated tissue or bodily fluids, such as through a medical procedure or eating contaminated beef (variant CJD).

There is no cure for Creutzfeldt-Jakob syndrome and it is fatal, usually within a year of onset of symptoms. Treatment focuses on managing the symptoms and making the patient as comfortable as possible.

The cerebellum is a part of the brain that lies behind the brainstem and is involved in the regulation of motor movements, balance, and coordination. It contains two hemispheres and a central portion called the vermis. The cerebellum receives input from sensory systems and other areas of the brain and spinal cord and sends output to motor areas of the brain. Damage to the cerebellum can result in problems with movement, balance, and coordination.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

Glial Fibrillary Acidic Protein (GFAP) is a type of intermediate filament protein that is primarily found in astrocytes, which are a type of star-shaped glial cells in the central nervous system (CNS). These proteins play an essential role in maintaining the structural integrity and stability of astrocytes. They also participate in various cellular processes such as responding to injury, providing support to neurons, and regulating the extracellular environment.

GFAP is often used as a marker for astrocytic activation or reactivity, which can occur in response to CNS injuries, neuroinflammation, or neurodegenerative diseases. Elevated GFAP levels in cerebrospinal fluid (CSF) or blood can indicate astrocyte damage or dysfunction and are associated with several neurological conditions, including traumatic brain injury, stroke, multiple sclerosis, Alzheimer's disease, and Alexander's disease.

Machado-Joseph Disease (MJD) is a genetic disorder that affects the part of the brain that controls movement. It is also known as spinocerebellar ataxia type 3 (SCA3). MJD is characterized by progressive problems with coordination, speech, and swallowing, along with muscle stiffness, tremors, and in some cases, eye movement abnormalities.

MJD is caused by a mutation in the ATXN3 gene, which results in an expanded CAG repeat sequence. This genetic defect leads to the production of an abnormal protein that accumulates in nerve cells, causing them to die. The severity and age of onset of MJD can vary widely, even within families, but symptoms typically begin between the ages of 10 and 60.

MJD is inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the disease-causing mutation from an affected parent. Currently, there is no cure for MJD, but treatments can help manage symptoms and improve quality of life.

Lysosomes are membrane-bound organelles found in the cytoplasm of eukaryotic cells. They are responsible for breaking down and recycling various materials, such as waste products, foreign substances, and damaged cellular components, through a process called autophagy or phagocytosis. Lysosomes contain hydrolytic enzymes that can break down biomolecules like proteins, nucleic acids, lipids, and carbohydrates into their basic building blocks, which can then be reused by the cell. They play a crucial role in maintaining cellular homeostasis and are often referred to as the "garbage disposal system" of the cell.

Nitro compounds, also known as nitro derivatives or nitro aromatics, are organic compounds that contain the nitro group (-NO2) bonded to an aromatic hydrocarbon ring. They are named as such because they contain a nitrogen atom in a -3 oxidation state and are typically prepared by the nitration of aromatic compounds using nitric acid or a mixture of nitric and sulfuric acids.

Nitro compounds have significant importance in organic chemistry due to their versatile reactivity, which allows for various chemical transformations. They can serve as useful intermediates in the synthesis of other chemical products, including dyes, pharmaceuticals, and explosives. However, some nitro compounds can also be hazardous, with potential health effects such as skin and respiratory irritation, and they may pose environmental concerns due to their persistence and potential toxicity.

It is important to handle nitro compounds with care, following appropriate safety guidelines and regulations, to minimize risks associated with their use.

Amyloidogenic proteins are misfolded proteins that can form amyloid fibrils, which are insoluble protein aggregates with a characteristic cross-beta sheet quaternary structure. These amyloid fibrils can accumulate in various tissues and organs, leading to the formation of amyloid deposits. The accumulation of amyloidogenic proteins and the resulting amyloid deposits have been associated with several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, as well as systemic amyloidoses.

In Alzheimer's disease, for example, the amyloidogenic protein is beta-amyloid, which is produced from the proteolytic processing of the amyloid precursor protein (APP). In Parkinson's disease, the amyloidogenic protein is alpha-synuclein, which forms the main component of Lewy bodies.

It's important to note that not all misfolded proteins are necessarily amyloidogenic, and not all amyloid fibrils are associated with disease. Some amyloid fibrils can have functional roles in normal physiological processes.

Dopamine is a type of neurotransmitter, which is a chemical messenger that transmits signals in the brain and nervous system. It plays several important roles in the body, including:

* Regulation of movement and coordination
* Modulation of mood and motivation
* Control of the reward and pleasure centers of the brain
* Regulation of muscle tone
* Involvement in memory and attention

Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area. It is released by neurons (nerve cells) and binds to specific receptors on other neurons, where it can either excite or inhibit their activity.

Abnormalities in dopamine signaling have been implicated in several neurological and psychiatric conditions, including Parkinson's disease, schizophrenia, and addiction.

1-Methyl-4-phenylpyridinium (MPP+) is a neurotoxic compound that is widely used in scientific research to study Parkinson's disease and other neurological disorders. MPP+ is an ionic form of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which is a lipophilic compound that can cross the blood-brain barrier and be converted to MPP+ by monoamine oxidase B (MAO-B) in glial cells.

MPP+ is taken up by dopaminergic neurons through the dopamine transporter (DAT), where it inhibits complex I of the electron transport chain, leading to mitochondrial dysfunction and energy depletion. This results in the death of dopaminergic neurons, which are the primary cells affected in Parkinson's disease.

MPP+ has been used as a model compound to study the mechanisms of neurodegeneration in Parkinson's disease and other neurological disorders, and it has also been used in the development of potential therapeutic strategies for these conditions.

Protein binding, in the context of medical and biological sciences, refers to the interaction between a protein and another molecule (known as the ligand) that results in a stable complex. This process is often reversible and can be influenced by various factors such as pH, temperature, and concentration of the involved molecules.

In clinical chemistry, protein binding is particularly important when it comes to drugs, as many of them bind to proteins (especially albumin) in the bloodstream. The degree of protein binding can affect a drug's distribution, metabolism, and excretion, which in turn influence its therapeutic effectiveness and potential side effects.

Protein-bound drugs may be less available for interaction with their target tissues, as only the unbound or "free" fraction of the drug is active. Therefore, understanding protein binding can help optimize dosing regimens and minimize adverse reactions.

Neurogenesis is the process by which new neurons (nerve cells) are generated in the brain. It occurs throughout life in certain areas of the brain, such as the hippocampus and subventricular zone, although the rate of neurogenesis decreases with age. Neurogenesis involves the proliferation, differentiation, and integration of new neurons into existing neural circuits. This process plays a crucial role in learning, memory, and recovery from brain injury or disease.

Cognitive disorders are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. These disorders can be caused by various factors such as brain injury, degenerative diseases, infection, substance abuse, or developmental disabilities. Examples of cognitive disorders include dementia, amnesia, delirium, and intellectual disability. It's important to note that the specific definition and diagnostic criteria for cognitive disorders may vary depending on the medical source or classification system being used.

Hormesis is a term used in medicine and toxicology to describe a biphasic dose response to a chemical or physical agent, where low doses induce a beneficial effect and high doses cause harm. It was first introduced in 1943 by biologist Antonius Van den Bergh.

In other words, hormesis describes the phenomenon where a substance that is toxic or harmful at high levels can have a stimulatory or protective effect at lower levels. This concept has been observed in various biological systems and across different species, including humans. The exact mechanisms behind hormesis are not fully understood, but it's believed to be related to the activation of stress response pathways that promote cellular protection and repair.

Examples of hormetic substances include some plant-derived compounds like resveratrol, found in grapes and red wine, which has been shown to have beneficial effects on cardiovascular health at low doses but can be toxic at high doses. Similarly, exposure to low levels of radiation has been suggested to stimulate DNA repair mechanisms, while high levels can cause damage and increase the risk of cancer.

It's important to note that hormesis is a complex phenomenon, and its application in medicine and public health remains controversial. Further research is needed to fully understand the underlying mechanisms and potential therapeutic applications of hormetic substances.

Brain diseases, also known as neurological disorders, refer to a wide range of conditions that affect the brain and nervous system. These diseases can be caused by various factors such as genetics, infections, injuries, degeneration, or structural abnormalities. They can affect different parts of the brain, leading to a variety of symptoms and complications.

Some examples of brain diseases include:

1. Alzheimer's disease - a progressive degenerative disorder that affects memory and cognitive function.
2. Parkinson's disease - a movement disorder characterized by tremors, stiffness, and difficulty with coordination and balance.
3. Multiple sclerosis - a chronic autoimmune disease that affects the nervous system and can cause a range of symptoms such as vision loss, muscle weakness, and cognitive impairment.
4. Epilepsy - a neurological disorder characterized by recurrent seizures.
5. Brain tumors - abnormal growths in the brain that can be benign or malignant.
6. Stroke - a sudden interruption of blood flow to the brain, which can cause paralysis, speech difficulties, and other neurological symptoms.
7. Meningitis - an infection of the membranes surrounding the brain and spinal cord.
8. Encephalitis - an inflammation of the brain that can be caused by viruses, bacteria, or autoimmune disorders.
9. Huntington's disease - a genetic disorder that affects muscle coordination, cognitive function, and mental health.
10. Migraine - a neurological condition characterized by severe headaches, often accompanied by nausea, vomiting, and sensitivity to light and sound.

Brain diseases can range from mild to severe and may be treatable or incurable. They can affect people of all ages and backgrounds, and early diagnosis and treatment are essential for improving outcomes and quality of life.

Spinocerebellar degenerations (SCDs) are a group of genetic disorders that primarily affect the cerebellum, the part of the brain responsible for coordinating muscle movements, and the spinal cord. These conditions are characterized by progressive degeneration or loss of nerve cells in the cerebellum and/or spinal cord, leading to various neurological symptoms.

SCDs are often inherited in an autosomal dominant manner, meaning that only one copy of the altered gene from either parent is enough to cause the disorder. The most common type of SCD is spinocerebellar ataxia (SCA), which includes several subtypes (SCA1, SCA2, SCA3, etc.) differentiated by their genetic causes and specific clinical features.

Symptoms of spinocerebellar degenerations may include:

1. Progressive ataxia (loss of coordination and balance)
2. Dysarthria (speech difficulty)
3. Nystagmus (involuntary eye movements)
4. Oculomotor abnormalities (problems with eye movement control)
5. Tremors or other involuntary muscle movements
6. Muscle weakness and spasticity
7. Sensory disturbances, such as numbness or tingling sensations
8. Dysphagia (difficulty swallowing)
9. Cognitive impairment in some cases

The age of onset, severity, and progression of symptoms can vary significantly among different SCD subtypes and individuals. Currently, there is no cure for spinocerebellar degenerations, but various supportive treatments and therapies can help manage symptoms and improve quality of life.

Neurotoxicity syndromes refer to a group of conditions caused by exposure to neurotoxins, which are substances that can damage the structure or function of the nervous system. Neurotoxicity syndromes can affect both the central and peripheral nervous systems and may cause a wide range of symptoms depending on the type and severity of the exposure.

Symptoms of neurotoxicity syndromes may include:

* Headache
* Dizziness
* Tremors or shaking
* Difficulty with coordination or balance
* Numbness or tingling in the hands and feet
* Vision problems
* Memory loss or difficulty concentrating
* Seizures or convulsions
* Mood changes, such as depression or anxiety

Neurotoxicity syndromes can be caused by exposure to a variety of substances, including heavy metals (such as lead, mercury, and arsenic), pesticides, solvents, and certain medications. In some cases, neurotoxicity syndromes may be reversible with treatment, while in other cases, the damage may be permanent.

Prevention is key in avoiding neurotoxicity syndromes, and it is important to follow safety guidelines when working with or around potential neurotoxins. If exposure does occur, prompt medical attention is necessary to minimize the risk of long-term health effects.

Medical Definition:

Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.

Scrapie is a progressive, fatal, degenerative disease affecting the central nervous system of sheep and goats. It is one of the transmissible spongiform encephalopathies (TSEs), also known as prion diseases. The agent responsible for scrapie is thought to be an abnormal form of the prion protein, which can cause normal prion proteins in the brain to adopt the abnormal shape and accumulate, leading to brain damage and neurodegeneration.

Scrapie is characterized by several clinical signs, including changes in behavior, tremors, loss of coordination, itching, and excessive scraping of the fleece against hard surfaces, which gives the disease its name. The incubation period for scrapie can range from 2 to 5 years, and there is no known treatment or cure for the disease.

Scrapie is not considered a significant threat to human health, but it has served as a model for understanding other prion diseases, such as bovine spongiform encephalopathy (BSE) in cattle, which can cause variant Creutzfeldt-Jakob disease (vCJD) in humans.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Wallerian degeneration is a process that occurs following damage to the axons of neurons (nerve cells). After an axon is severed or traumatically injured, it undergoes a series of changes including fragmentation and removal of the distal segment of the axon, which is the part that is separated from the cell body. This process is named after Augustus Waller, who first described it in 1850.

The degenerative changes in the distal axon are characterized by the breakdown of the axonal cytoskeleton, the loss of myelin sheath (the fatty insulating material that surrounds and protects the axon), and the infiltration of macrophages to clear away the debris. These events lead to the degeneration of the distal axon segment, which is necessary for successful regeneration of the injured nerve.

Wallerian degeneration is a crucial process in the nervous system's response to injury, as it enables the regrowth of axons and the reestablishment of connections between neurons. However, if the regenerative capacity of the neuron is insufficient or the environment is not conducive to growth, functional recovery may be impaired, leading to long-term neurological deficits.

Gamma-synuclein is a protein that belongs to the synuclein family, which also includes alpha-synuclein and beta-synuclein. These proteins are abundantly expressed in the brain and are involved in various cellular processes such as vesicle trafficking, neurotransmitter release, and maintaining the structure of neurons.

Gamma-synuclein is primarily found in the central nervous system and is expressed at lower levels compared to alpha-synuclein. It has been identified as a component of Lewy bodies, which are intracellular inclusions found in the brains of patients with Parkinson's disease and other synucleinopathies. However, its precise role in these diseases remains unclear.

Like other synucleins, gamma-synuclein can form aggregates under certain conditions, and this property has been suggested to contribute to its pathological role in neurodegenerative disorders. Additionally, gamma-synuclein has been implicated in cancer, where it promotes tumor growth and metastasis.

Overall, further research is needed to fully understand the physiological and pathological functions of gamma-synuclein.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a chemical compound that can cause permanent parkinsonian symptoms. It is not a medication or a treatment, but rather a toxin that can damage the dopamine-producing neurons in the brain, leading to symptoms similar to those seen in Parkinson's disease.

MPTP itself is not harmful, but it is metabolized in the body into a toxic compound called MPP+, which accumulates in and damages dopaminergic neurons. MPTP was discovered in the 1980s when a group of drug users in California developed parkinsonian symptoms after injecting a heroin-like substance contaminated with MPTP.

Since then, MPTP has been used as a research tool to study Parkinson's disease and develop new treatments. However, it is not used clinically and should be handled with caution due to its toxicity.

Brain chemistry refers to the chemical processes that occur within the brain, particularly those involving neurotransmitters, neuromodulators, and neuropeptides. These chemicals are responsible for transmitting signals between neurons (nerve cells) in the brain, allowing for various cognitive, emotional, and physical functions.

Neurotransmitters are chemical messengers that transmit signals across the synapse (the tiny gap between two neurons). Examples of neurotransmitters include dopamine, serotonin, norepinephrine, GABA (gamma-aminobutyric acid), and glutamate. Each neurotransmitter has a specific role in brain function, such as regulating mood, motivation, attention, memory, and movement.

Neuromodulators are chemicals that modify the effects of neurotransmitters on neurons. They can enhance or inhibit the transmission of signals between neurons, thereby modulating brain activity. Examples of neuromodulators include acetylcholine, histamine, and substance P.

Neuropeptides are small protein-like molecules that act as neurotransmitters or neuromodulators. They play a role in various physiological functions, such as pain perception, stress response, and reward processing. Examples of neuropeptides include endorphins, enkephalins, and oxytocin.

Abnormalities in brain chemistry can lead to various neurological and psychiatric conditions, such as depression, anxiety disorders, schizophrenia, Parkinson's disease, and Alzheimer's disease. Understanding brain chemistry is crucial for developing effective treatments for these conditions.

PC12 cells are a type of rat pheochromocytoma cell line, which are commonly used in scientific research. Pheochromocytomas are tumors that develop from the chromaffin cells of the adrenal gland, and PC12 cells are a subtype of these cells.

PC12 cells have several characteristics that make them useful for research purposes. They can be grown in culture and can be differentiated into a neuron-like phenotype when treated with nerve growth factor (NGF). This makes them a popular choice for studies involving neuroscience, neurotoxicity, and neurodegenerative disorders.

PC12 cells are also known to express various neurotransmitter receptors, ion channels, and other proteins that are relevant to neuronal function, making them useful for studying the mechanisms of drug action and toxicity. Additionally, PC12 cells can be used to study the regulation of cell growth and differentiation, as well as the molecular basis of cancer.

A mutant protein is a protein that has undergone a genetic mutation, resulting in an altered amino acid sequence and potentially changed structure and function. These changes can occur due to various reasons such as errors during DNA replication, exposure to mutagenic substances, or inherited genetic disorders. The alterations in the protein's structure and function may have no significant effects, lead to benign phenotypic variations, or cause diseases, depending on the type and location of the mutation. Some well-known examples of diseases caused by mutant proteins include cystic fibrosis, sickle cell anemia, and certain types of cancer.

Medical Definition:
Microtubule-associated proteins (MAPs) are a diverse group of proteins that bind to microtubules, which are key components of the cytoskeleton in eukaryotic cells. MAPs play crucial roles in regulating microtubule dynamics and stability, as well as in mediating interactions between microtubules and other cellular structures. They can be classified into several categories based on their functions, including:

1. Microtubule stabilizers: These MAPs promote the assembly of microtubules and protect them from disassembly by enhancing their stability. Examples include tau proteins and MAP2.
2. Microtubule dynamics regulators: These MAPs modulate the rate of microtubule polymerization and depolymerization, allowing for dynamic reorganization of the cytoskeleton during cell division and other processes. Examples include stathmin and XMAP215.
3. Microtubule motor proteins: These MAPs use energy from ATP hydrolysis to move along microtubules, transporting various cargoes within the cell. Examples include kinesin and dynein.
4. Adapter proteins: These MAPs facilitate interactions between microtubules and other cellular structures, such as membranes, organelles, or signaling molecules. Examples include MAP4 and CLASPs.

Dysregulation of MAPs has been implicated in several diseases, including neurodegenerative disorders like Alzheimer's disease (where tau proteins form abnormal aggregates called neurofibrillary tangles) and cancer (where altered microtubule dynamics can contribute to uncontrolled cell division).

Mitochondrial proteins are any proteins that are encoded by the nuclear genome or mitochondrial genome and are located within the mitochondria, an organelle found in eukaryotic cells. These proteins play crucial roles in various cellular processes including energy production, metabolism of lipids, amino acids, and steroids, regulation of calcium homeostasis, and programmed cell death or apoptosis.

Mitochondrial proteins can be classified into two main categories based on their origin:

1. Nuclear-encoded mitochondrial proteins (NEMPs): These are proteins that are encoded by genes located in the nucleus, synthesized in the cytoplasm, and then imported into the mitochondria through specific import pathways. NEMPs make up about 99% of all mitochondrial proteins and are involved in various functions such as oxidative phosphorylation, tricarboxylic acid (TCA) cycle, fatty acid oxidation, and mitochondrial dynamics.

2. Mitochondrial DNA-encoded proteins (MEPs): These are proteins that are encoded by the mitochondrial genome, synthesized within the mitochondria, and play essential roles in the electron transport chain (ETC), a key component of oxidative phosphorylation. The human mitochondrial genome encodes only 13 proteins, all of which are subunits of complexes I, III, IV, and V of the ETC.

Defects in mitochondrial proteins can lead to various mitochondrial disorders, which often manifest as neurological, muscular, or metabolic symptoms due to impaired energy production. These disorders are usually caused by mutations in either nuclear or mitochondrial genes that encode mitochondrial proteins.

Protein transport, in the context of cellular biology, refers to the process by which proteins are actively moved from one location to another within or between cells. This is a crucial mechanism for maintaining proper cell function and regulation.

Intracellular protein transport involves the movement of proteins within a single cell. Proteins can be transported across membranes (such as the nuclear envelope, endoplasmic reticulum, Golgi apparatus, or plasma membrane) via specialized transport systems like vesicles and transport channels.

Intercellular protein transport refers to the movement of proteins from one cell to another, often facilitated by exocytosis (release of proteins in vesicles) and endocytosis (uptake of extracellular substances via membrane-bound vesicles). This is essential for communication between cells, immune response, and other physiological processes.

It's important to note that any disruption in protein transport can lead to various diseases, including neurological disorders, cancer, and metabolic conditions.

Oxidopamine is not a recognized medical term or a medication commonly used in clinical practice. However, it is a chemical compound that is often used in scientific research, particularly in the field of neuroscience.

Oxidopamine is a synthetic catecholamine that can be selectively taken up by dopaminergic neurons and subsequently undergo oxidation, leading to the production of reactive oxygen species. This property makes it a useful tool for studying the effects of oxidative stress on dopaminergic neurons in models of Parkinson's disease and other neurological disorders.

In summary, while not a medical definition per se, oxidopamine is a chemical compound used in research to study the effects of oxidative stress on dopaminergic neurons.

Inflammation is a complex biological response of tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is characterized by the following signs: rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function). The process involves the activation of the immune system, recruitment of white blood cells, and release of inflammatory mediators, which contribute to the elimination of the injurious stimuli and initiation of the healing process. However, uncontrolled or chronic inflammation can also lead to tissue damage and diseases.

Niemann-Pick Disease, Type C (NPC) is a rare, progressive, and fatal neurovisceral lipid storage disorder caused by mutations in the NPC1 or NPC2 genes. These genetic defects result in impaired intracellular transport of cholesterol and other lipids, leading to excessive accumulation within lysosomes of various tissues, particularly in the brain, liver, spleen, and lungs.

The disease primarily affects children, although late-onset forms have been reported in adults. The symptoms and severity can vary widely among patients but often include neurological manifestations such as ataxia, dysarthria, dysphagia, cognitive decline, seizures, and vertical supranuclear gaze palsy (VSGP). Other features may involve visceral involvement like hepatosplenomegaly, jaundice, or pulmonary complications.

There is currently no cure for NPC, but treatments aim to manage symptoms, slow disease progression, and improve quality of life. Miglustat and cyclodextrin (HPβCD) are two FDA-approved therapeutic options that have shown some promise in stabilizing or delaying neurological decline in NPC patients. Early diagnosis and intervention are crucial for optimizing outcomes and providing appropriate supportive care.

Green Fluorescent Protein (GFP) is not a medical term per se, but a scientific term used in the field of molecular biology. GFP is a protein that exhibits bright green fluorescence when exposed to light, particularly blue or ultraviolet light. It was originally discovered in the jellyfish Aequorea victoria.

In medical and biological research, scientists often use recombinant DNA technology to introduce the gene for GFP into other organisms, including bacteria, plants, and animals, including humans. This allows them to track the expression and localization of specific genes or proteins of interest in living cells, tissues, or even whole organisms.

The ability to visualize specific cellular structures or processes in real-time has proven invaluable for a wide range of research areas, from studying the development and function of organs and organ systems to understanding the mechanisms of diseases and the effects of therapeutic interventions.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Serine proteases are a type of enzyme that cleaves peptide bonds in proteins. They have a serine residue in their active site that plays a crucial role in the catalytic mechanism. These enzymes are involved in various biological processes, including blood coagulation, fibrinolysis, inflammation, cell death, and hormone activation. Some examples of serine proteases include trypsin, chymotrypsin, thrombin, and elastase. They play a significant role in disease processes such as cancer, Alzheimer's disease, and emphysema.

Glutamic acid is an alpha-amino acid, which is one of the 20 standard amino acids in the genetic code. The systematic name for this amino acid is (2S)-2-Aminopentanedioic acid. Its chemical formula is HO2CCH(NH2)CH2CH2CO2H.

Glutamic acid is a crucial excitatory neurotransmitter in the human brain, and it plays an essential role in learning and memory. It's also involved in the metabolism of sugars and amino acids, the synthesis of proteins, and the removal of waste nitrogen from the body.

Glutamic acid can be found in various foods such as meat, fish, beans, eggs, dairy products, and vegetables. In the human body, glutamic acid can be converted into gamma-aminobutyric acid (GABA), another important neurotransmitter that has a calming effect on the nervous system.

Fatal Familial Insomnia (FFI) is a rare, inherited prion disease characterized by progressive insomnia that leads to death, typically within a year of onset. It is caused by a mutation in the PRNP gene, which encodes the prion protein. The mutation results in an abnormal form of the prion protein that accumulates in the brain and causes damage to nerve cells.

The symptoms of FFI usually begin in middle age and include progressive insomnia, rapid weight loss, hallucinations, confusion, and eventually dementia. As the disease progresses, patients may experience muscle spasms, rigidity, and difficulty swallowing. There is no cure for FFI, and treatment is focused on managing symptoms and providing supportive care.

FFI is inherited in an autosomal dominant manner, meaning that a person has a 50% chance of inheriting the mutated gene from an affected parent. The disease affects both men and women and has been reported in families worldwide.

"Drosophila" is a genus of small flies, also known as fruit flies. The most common species used in scientific research is "Drosophila melanogaster," which has been a valuable model organism for many areas of biological and medical research, including genetics, developmental biology, neurobiology, and aging.

The use of Drosophila as a model organism has led to numerous important discoveries in genetics and molecular biology, such as the identification of genes that are associated with human diseases like cancer, Parkinson's disease, and obesity. The short reproductive cycle, large number of offspring, and ease of genetic manipulation make Drosophila a powerful tool for studying complex biological processes.

Brain-Derived Neurotrophic Factor (BDNF) is a type of protein called a neurotrophin, which is involved in the growth and maintenance of neurons (nerve cells) in the brain. BDNFA is encoded by the BDNF gene and is widely expressed throughout the central nervous system. It plays an essential role in supporting the survival of existing neurons, encouraging the growth and differentiation of new neurons and synapses, and contributing to neuroplasticity - the ability of the brain to change and adapt as a result of experience. Low levels of BDNF have been associated with several neurological disorders, including depression, Alzheimer's disease, and Huntington's disease.

The Blood-Brain Barrier (BBB) is a highly specialized, selective interface between the central nervous system (CNS) and the circulating blood. It is formed by unique endothelial cells that line the brain's capillaries, along with tight junctions, astrocytic foot processes, and pericytes, which together restrict the passage of substances from the bloodstream into the CNS. This barrier serves to protect the brain from harmful agents and maintain a stable environment for proper neural function. However, it also poses a challenge in delivering therapeutics to the CNS, as most large and hydrophilic molecules cannot cross the BBB.

A peptide fragment is a short chain of amino acids that is derived from a larger peptide or protein through various biological or chemical processes. These fragments can result from the natural breakdown of proteins in the body during regular physiological processes, such as digestion, or they can be produced experimentally in a laboratory setting for research or therapeutic purposes.

Peptide fragments are often used in research to map the structure and function of larger peptides and proteins, as well as to study their interactions with other molecules. In some cases, peptide fragments may also have biological activity of their own and can be developed into drugs or diagnostic tools. For example, certain peptide fragments derived from hormones or neurotransmitters may bind to receptors in the body and mimic or block the effects of the full-length molecule.

Phosphorylation is the process of adding a phosphate group (a molecule consisting of one phosphorus atom and four oxygen atoms) to a protein or other organic molecule, which is usually done by enzymes called kinases. This post-translational modification can change the function, localization, or activity of the target molecule, playing a crucial role in various cellular processes such as signal transduction, metabolism, and regulation of gene expression. Phosphorylation is reversible, and the removal of the phosphate group is facilitated by enzymes called phosphatases.

Mitochondrial dynamics refer to the processes that regulate the shape, size, distribution, and quality control of mitochondria within cells. These dynamic processes include:

1. Mitochondrial Fusion: This is the process by which two adjacent mitochondria merge together to form a single, elongated organelle. Fusion allows for the exchange of mitochondrial content, including DNA, proteins, and metabolites, which helps maintain genetic stability and promote bioenergetic efficiency.
2. Mitochondrial Fission: This is the process by which a single mitochondrion divides into two separate organelles. Fission plays a crucial role in mitochondrial division, inheritance, and quality control, as it enables the segregation of damaged or dysfunctional mitochondria for degradation via autophagy (mitophagy).
3. Mitochondrial Transport: This is the active movement of mitochondria within cells, facilitated by cytoskeletal motor proteins. Mitochondrial transport enables organelles to be distributed evenly throughout the cell and to reach specific subcellular locations where their energy demands are high.
4. Mitochondrial Dynamics Regulation: The regulation of mitochondrial dynamics involves a complex interplay between various proteins, lipids, and signaling pathways that control fusion, fission, transport, and quality control processes. These regulatory mechanisms help maintain the balance between mitochondrial biogenesis (the generation of new organelles) and mitophagy (the removal of damaged ones), ensuring proper cellular homeostasis and function.

Dysregulation of mitochondrial dynamics has been implicated in various pathological conditions, including neurodegenerative diseases, metabolic disorders, and aging-related processes.

"Silver staining" is a histological term that refers to a technique used to selectively stain various components of biological tissues, making them more visible under a microscope. This technique is often used in the study of histopathology and cytology. The most common type of silver staining is known as "silver impregnation," which is used to demonstrate the presence of argyrophilic structures, such as nerve fibers and neurofibrillary tangles, in tissues.

The process of silver staining involves the use of silver salts, which are reduced by a developer to form metallic silver that deposits on the tissue components. The intensity of the stain depends on the degree of reduction of the silver ions, and it can be modified by adjusting the concentration of the silver salt, the development time, and other factors.

Silver staining is widely used in diagnostic pathology to highlight various structures such as nerve fibers, axons, collagen, basement membranes, and microorganisms like fungi and bacteria. It has also been used in research to study the distribution and organization of these structures in tissues. However, it's important to note that silver staining is not specific for any particular substance, so additional tests are often needed to confirm the identity of the stained structures.

Rotenone is not strictly a medical term, but it is a pesticide that is used in some medical situations. According to the National Pesticide Information Center, rotenone is a pesticide derived from the roots and stems of several plants, including Derris Eliptica, Lonchocarpus utilis, and Tephrosia vogelii. It is used as a pesticide to control insects, mites, and fish in both agricultural and residential settings.

In medical contexts, rotenone has been studied for its potential effects on human health, particularly in relation to Parkinson's disease. Some research suggests that exposure to rotenone may increase the risk of developing Parkinson's disease, although more studies are needed to confirm this link. Rotenone works by inhibiting the mitochondria in cells, which can lead to cell death and neurodegeneration.

It is important to note that rotenone is highly toxic and should be handled with care. It can cause skin and eye irritation, respiratory problems, and gastrointestinal symptoms if ingested or inhaled. Therefore, it is recommended to use personal protective equipment when handling rotenone and to follow all label instructions carefully.

Thiol esters are chemical compounds that contain a sulfur atom (from a mercapto group, -SH) linked to a carbonyl group (a carbon double-bonded to an oxygen atom, -CO-) through an ester bond. Thiolester hydrolases are enzymes that catalyze the hydrolysis of thiol esters, breaking down these compounds into a carboxylic acid and a thiol (a compound containing a mercapto group).

In biological systems, thiolester bonds play important roles in various metabolic pathways. For example, acetyl-CoA, a crucial molecule in energy metabolism, is a thiol ester that forms between coenzyme A and an acetyl group. Thiolester hydrolases help regulate the formation and breakdown of these thiol esters, allowing cells to control various biochemical reactions.

Examples of thiolester hydrolases include:

1. CoA thioesterases (CoATEs): These enzymes hydrolyze thiol esters between coenzyme A and fatty acids, releasing free coenzyme A and a fatty acid. This process is essential for fatty acid metabolism.
2. Acetyl-CoA hydrolase: This enzyme specifically breaks down the thiol ester bond in acetyl-CoA, releasing acetic acid and coenzyme A.
3. Thioesterases involved in non-ribosomal peptide synthesis (NRPS): These enzymes hydrolyze thiol esters during the biosynthesis of complex peptides, allowing for the formation of unique amino acid sequences and structures.

Understanding the function and regulation of thiolester hydrolases can provide valuable insights into various metabolic processes and potential therapeutic targets in disease treatment.

Analysis of Variance (ANOVA) is a statistical technique used to compare the means of two or more groups and determine whether there are any significant differences between them. It is a way to analyze the variance in a dataset to determine whether the variability between groups is greater than the variability within groups, which can indicate that the groups are significantly different from one another.

ANOVA is based on the concept of partitioning the total variance in a dataset into two components: variance due to differences between group means (also known as "between-group variance") and variance due to differences within each group (also known as "within-group variance"). By comparing these two sources of variance, ANOVA can help researchers determine whether any observed differences between groups are statistically significant, or whether they could have occurred by chance.

ANOVA is a widely used technique in many areas of research, including biology, psychology, engineering, and business. It is often used to compare the means of two or more experimental groups, such as a treatment group and a control group, to determine whether the treatment had a significant effect. ANOVA can also be used to compare the means of different populations or subgroups within a population, to identify any differences that may exist between them.

'Animal behavior' refers to the actions or responses of animals to various stimuli, including their interactions with the environment and other individuals. It is the study of the actions of animals, whether they are instinctual, learned, or a combination of both. Animal behavior includes communication, mating, foraging, predator avoidance, and social organization, among other things. The scientific study of animal behavior is called ethology. This field seeks to understand the evolutionary basis for behaviors as well as their physiological and psychological mechanisms.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Hereditary Spastic Paraplegia (HSP) is a group of genetic disorders that affect the long motor neurons in the spinal cord, leading to lower limb spasticity and weakness. It is characterized by progressive stiffness and contraction of the leg muscles, resulting in difficulty with walking and balance.

The symptoms of HSP typically begin in childhood or early adulthood and worsen over time. The severity of the condition can vary widely, even within the same family, depending on the specific genetic mutation involved. In addition to lower limb spasticity, some individuals with HSP may also experience bladder dysfunction, sensory loss, or other neurological symptoms.

HSP is inherited in an autosomal dominant or autosomal recessive pattern, depending on the specific genetic mutation involved. There are over 70 different genes that have been identified as causing HSP, and genetic testing can be used to confirm the diagnosis and identify the specific genetic mutation responsible.

Treatment for HSP is focused on managing symptoms and maintaining mobility. Physical therapy, orthotics, and medications such as baclofen or tizanidine may be used to help reduce muscle spasticity and improve mobility. In some cases, surgery may be necessary to relieve muscle contractures or other complications.

Cytoprotection refers to the protection of cells, particularly from harmful agents or damaging conditions. This can be achieved through various mechanisms, such as:

1. Activation of cellular defense pathways that help cells resist damage.
2. Inhibition of oxidative stress and inflammation, which can cause cellular damage.
3. Enhancement of cell repair processes, enabling cells to recover from damage more effectively.
4. Prevention of apoptosis (programmed cell death) or promotion of cell survival signals.

In the medical context, cytoprotective agents are often used to protect tissues and organs from injury due to various factors like chemotherapy, radiation therapy, ischemia-reperfusion injury, or inflammation. These agents can include antioxidants, anti-inflammatory drugs, growth factors, and other compounds that help maintain cellular integrity and function.

Protein multimerization refers to the process where multiple protein subunits assemble together to form a complex, repetitive structure called a multimer or oligomer. This can involve the association of identical or similar protein subunits through non-covalent interactions such as hydrogen bonding, ionic bonding, and van der Waals forces. The resulting multimeric structures can have various shapes, sizes, and functions, including enzymatic activity, transport, or structural support. Protein multimerization plays a crucial role in many biological processes and is often necessary for the proper functioning of proteins within cells.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Neural stem cells (NSCs) are a type of undifferentiated cells found in the central nervous system, including the brain and spinal cord. They have the ability to self-renew and generate the main types of cells found in the nervous system, such as neurons, astrocytes, and oligodendrocytes. NSCs are capable of dividing symmetrically to increase their own population or asymmetrically to produce one stem cell and one differentiated cell. They play a crucial role in the development and maintenance of the nervous system, and have the potential to be used in regenerative medicine and therapies for neurological disorders and injuries.

Proteolysis is the biological process of breaking down proteins into smaller polypeptides or individual amino acids by the action of enzymes called proteases. This process is essential for various physiological functions, including digestion, protein catabolism, cell signaling, and regulation of numerous biological activities. Dysregulation of proteolysis can contribute to several pathological conditions, such as cancer, neurodegenerative diseases, and inflammatory disorders.

Transmission electron microscopy (TEM) is a type of microscopy in which an electron beam is transmitted through a ultra-thin specimen, interacting with it as it passes through. An image is formed from the interaction of the electrons with the specimen; the image is then magnified and visualized on a fluorescent screen or recorded on an electronic detector (or photographic film in older models).

TEM can provide high-resolution, high-magnification images that can reveal the internal structure of specimens including cells, viruses, and even molecules. It is widely used in biological and materials science research to investigate the ultrastructure of cells, tissues and materials. In medicine, TEM is used for diagnostic purposes in fields such as virology and bacteriology.

It's important to note that preparing a sample for TEM is a complex process, requiring specialized techniques to create thin (50-100 nm) specimens. These include cutting ultrathin sections of embedded samples using an ultramicrotome, staining with heavy metal salts, and positive staining or negative staining methods.

"Motor activity" is a general term used in the field of medicine and neuroscience to refer to any kind of physical movement or action that is generated by the body's motor system. The motor system includes the brain, spinal cord, nerves, and muscles that work together to produce movements such as walking, talking, reaching for an object, or even subtle actions like moving your eyes.

Motor activity can be voluntary, meaning it is initiated intentionally by the individual, or involuntary, meaning it is triggered automatically by the nervous system without conscious control. Examples of voluntary motor activity include deliberately lifting your arm or kicking a ball, while examples of involuntary motor activity include heartbeat, digestion, and reflex actions like jerking your hand away from a hot stove.

Abnormalities in motor activity can be a sign of neurological or muscular disorders, such as Parkinson's disease, cerebral palsy, or multiple sclerosis. Assessment of motor activity is often used in the diagnosis and treatment of these conditions.

Purkinje cells are a type of neuron located in the cerebellar cortex, which is the outer layer of the cerebellum, a part of the brain that plays a crucial role in motor control and coordination. These cells have large branching dendrites and receive input from many other neurons, particularly granule cells. The axons of Purkinje cells form the principal output pathway of the cerebellar cortex, synapsing with deep cerebellar nuclei. They are named after Johannes Evangelista Purkinje, a Czech physiologist who first described them in 1837.

Methyl-phenyl-tetrahydropyridine (MPTP) poisoning is a rare neurological disorder that occurs due to the accidental exposure or intentional intake of MPTP, a chemical compound that can cause permanent parkinsonian symptoms. MPTP is metabolized into MPP+, which selectively destroys dopaminergic neurons in the substantia nigra pars compacta region of the brain, leading to Parkinson's disease-like features such as rigidity, bradykinesia, resting tremors, and postural instability. MPTP poisoning can be a model for understanding Parkinson's disease pathophysiology and developing potential treatments.

Disease progression is the worsening or advancement of a medical condition over time. It refers to the natural course of a disease, including its development, the severity of symptoms and complications, and the impact on the patient's overall health and quality of life. Understanding disease progression is important for developing appropriate treatment plans, monitoring response to therapy, and predicting outcomes.

The rate of disease progression can vary widely depending on the type of medical condition, individual patient factors, and the effectiveness of treatment. Some diseases may progress rapidly over a short period of time, while others may progress more slowly over many years. In some cases, disease progression may be slowed or even halted with appropriate medical interventions, while in other cases, the progression may be inevitable and irreversible.

In clinical practice, healthcare providers closely monitor disease progression through regular assessments, imaging studies, and laboratory tests. This information is used to guide treatment decisions and adjust care plans as needed to optimize patient outcomes and improve quality of life.

A missense mutation is a type of point mutation in which a single nucleotide change results in the substitution of a different amino acid in the protein that is encoded by the affected gene. This occurs when the altered codon (a sequence of three nucleotides that corresponds to a specific amino acid) specifies a different amino acid than the original one. The function and/or stability of the resulting protein may be affected, depending on the type and location of the missense mutation. Missense mutations can have various effects, ranging from benign to severe, depending on the importance of the changed amino acid for the protein's structure or function.

Group III histone deacetylases (HDACs) are a subfamily of enzymes that remove acetyl groups from lysine residues on histone proteins, which make up the structural core of chromatin in eukaryotic cells. This deacetylation results in a more compact and condensed chromatin structure, which typically leads to transcriptional repression of genes.

Group III HDACs specifically include HDACs 8 and 10. These enzymes are characterized by their unique domain organization and sequence homology. Unlike other HDAC families, Group III HDACs do not require zinc for their catalytic activity and instead utilize a conserved NAD+-binding site. This distinctive feature allows them to be inhibited by NAD+ analogs, which has led to the development of potential therapeutic strategies for various diseases, including cancer.

HDAC8 is widely expressed in different tissues and has been implicated in several cellular processes, such as transcriptional regulation, chromatin remodeling, and cell cycle progression. Mutations in HDAC8 have been associated with developmental disorders, such as Cornelia de Lange syndrome.

HDAC10 is also expressed in various tissues and has been shown to play roles in regulating autophagy, DNA damage response, and inflammation. Dysregulation of Group III HDACs has been linked to the pathogenesis of several diseases, including cancer, neurodegenerative disorders, and cardiovascular diseases.

A synapse is a structure in the nervous system that allows for the transmission of signals from one neuron (nerve cell) to another. It is the point where the axon terminal of one neuron meets the dendrite or cell body of another, and it is here that neurotransmitters are released and received. The synapse includes both the presynaptic and postsynaptic elements, as well as the cleft between them.

At the presynaptic side, an action potential travels down the axon and triggers the release of neurotransmitters into the synaptic cleft through exocytosis. These neurotransmitters then bind to receptors on the postsynaptic side, which can either excite or inhibit the receiving neuron. The strength of the signal between two neurons is determined by the number and efficiency of these synapses.

Synapses play a crucial role in the functioning of the nervous system, allowing for the integration and processing of information from various sources. They are also dynamic structures that can undergo changes in response to experience or injury, which has important implications for learning, memory, and recovery from neurological disorders.

Quaternary protein structure refers to the arrangement and interaction of multiple folded protein molecules in a multi-subunit complex. These subunits can be identical or different forms of the same protein or distinctly different proteins that associate to form a functional complex. The quaternary structure is held together by non-covalent interactions, such as hydrogen bonds, ionic bonds, and van der Waals forces. Understanding quaternary structure is crucial for comprehending the function, regulation, and assembly of many protein complexes involved in various cellular processes.

A biological marker, often referred to as a biomarker, is a measurable indicator that reflects the presence or severity of a disease state, or a response to a therapeutic intervention. Biomarkers can be found in various materials such as blood, tissues, or bodily fluids, and they can take many forms, including molecular, histologic, radiographic, or physiological measurements.

In the context of medical research and clinical practice, biomarkers are used for a variety of purposes, such as:

1. Diagnosis: Biomarkers can help diagnose a disease by indicating the presence or absence of a particular condition. For example, prostate-specific antigen (PSA) is a biomarker used to detect prostate cancer.
2. Monitoring: Biomarkers can be used to monitor the progression or regression of a disease over time. For instance, hemoglobin A1c (HbA1c) levels are monitored in diabetes patients to assess long-term blood glucose control.
3. Predicting: Biomarkers can help predict the likelihood of developing a particular disease or the risk of a negative outcome. For example, the presence of certain genetic mutations can indicate an increased risk for breast cancer.
4. Response to treatment: Biomarkers can be used to evaluate the effectiveness of a specific treatment by measuring changes in the biomarker levels before and after the intervention. This is particularly useful in personalized medicine, where treatments are tailored to individual patients based on their unique biomarker profiles.

It's important to note that for a biomarker to be considered clinically valid and useful, it must undergo rigorous validation through well-designed studies, including demonstrating sensitivity, specificity, reproducibility, and clinical relevance.

Oxidation-Reduction (redox) reactions are a type of chemical reaction involving a transfer of electrons between two species. The substance that loses electrons in the reaction is oxidized, and the substance that gains electrons is reduced. Oxidation and reduction always occur together in a redox reaction, hence the term "oxidation-reduction."

In biological systems, redox reactions play a crucial role in many cellular processes, including energy production, metabolism, and signaling. The transfer of electrons in these reactions is often facilitated by specialized molecules called electron carriers, such as nicotinamide adenine dinucleotide (NAD+/NADH) and flavin adenine dinucleotide (FAD/FADH2).

The oxidation state of an element in a compound is a measure of the number of electrons that have been gained or lost relative to its neutral state. In redox reactions, the oxidation state of one or more elements changes as they gain or lose electrons. The substance that is oxidized has a higher oxidation state, while the substance that is reduced has a lower oxidation state.

Overall, oxidation-reduction reactions are fundamental to the functioning of living organisms and are involved in many important biological processes.

DNA-binding proteins are a type of protein that have the ability to bind to DNA (deoxyribonucleic acid), the genetic material of organisms. These proteins play crucial roles in various biological processes, such as regulation of gene expression, DNA replication, repair and recombination.

The binding of DNA-binding proteins to specific DNA sequences is mediated by non-covalent interactions, including electrostatic, hydrogen bonding, and van der Waals forces. The specificity of binding is determined by the recognition of particular nucleotide sequences or structural features of the DNA molecule.

DNA-binding proteins can be classified into several categories based on their structure and function, such as transcription factors, histones, and restriction enzymes. Transcription factors are a major class of DNA-binding proteins that regulate gene expression by binding to specific DNA sequences in the promoter region of genes and recruiting other proteins to modulate transcription. Histones are DNA-binding proteins that package DNA into nucleosomes, the basic unit of chromatin structure. Restriction enzymes are DNA-binding proteins that recognize and cleave specific DNA sequences, and are widely used in molecular biology research and biotechnology applications.

Proteins are complex, large molecules that play critical roles in the body's functions. They are made up of amino acids, which are organic compounds that are the building blocks of proteins. Proteins are required for the structure, function, and regulation of the body's tissues and organs. They are essential for the growth, repair, and maintenance of body tissues, and they play a crucial role in many biological processes, including metabolism, immune response, and cellular signaling. Proteins can be classified into different types based on their structure and function, such as enzymes, hormones, antibodies, and structural proteins. They are found in various foods, especially animal-derived products like meat, dairy, and eggs, as well as plant-based sources like beans, nuts, and grains.

'Drosophila melanogaster' is the scientific name for a species of fruit fly that is commonly used as a model organism in various fields of biological research, including genetics, developmental biology, and evolutionary biology. Its small size, short generation time, large number of offspring, and ease of cultivation make it an ideal subject for laboratory studies. The fruit fly's genome has been fully sequenced, and many of its genes have counterparts in the human genome, which facilitates the understanding of genetic mechanisms and their role in human health and disease.

Here is a brief medical definition:

Drosophila melanogaster (droh-suh-fih-luh meh-lon-guh-ster): A species of fruit fly used extensively as a model organism in genetic, developmental, and evolutionary research. Its genome has been sequenced, revealing many genes with human counterparts, making it valuable for understanding genetic mechanisms and their role in human health and disease.

HEK293 cells, also known as human embryonic kidney 293 cells, are a line of cells used in scientific research. They were originally derived from human embryonic kidney cells and have been adapted to grow in a lab setting. HEK293 cells are widely used in molecular biology and biochemistry because they can be easily transfected (a process by which DNA is introduced into cells) and highly express foreign genes. As a result, they are often used to produce proteins for structural and functional studies. It's important to note that while HEK293 cells are derived from human tissue, they have been grown in the lab for many generations and do not retain the characteristics of the original embryonic kidney cells.

Ubiquitin-protein ligases, also known as E3 ubiquitin ligases, are a group of enzymes that play a crucial role in the ubiquitination process. Ubiquitination is a post-translational modification where ubiquitin molecules are attached to specific target proteins, marking them for degradation by the proteasome or for other regulatory functions.

Ubiquitin-protein ligases catalyze the final step in this process by binding to both the ubiquitin protein and the target protein, facilitating the transfer of ubiquitin from an E2 ubiquitin-conjugating enzyme to the target protein. There are several different types of ubiquitin-protein ligases, each with their own specificity for particular target proteins and regulatory functions.

Ubiquitin-protein ligases have been implicated in various cellular processes such as protein degradation, DNA repair, signal transduction, and regulation of the cell cycle. Dysregulation of ubiquitination has been associated with several diseases, including cancer, neurodegenerative disorders, and inflammatory responses. Therefore, understanding the function and regulation of ubiquitin-protein ligases is an important area of research in biology and medicine.

The mesencephalon, also known as the midbrain, is the middle portion of the brainstem that connects the hindbrain (rhombencephalon) and the forebrain (prosencephalon). It plays a crucial role in several important functions including motor control, vision, hearing, and the regulation of consciousness and sleep-wake cycles. The mesencephalon contains several important structures such as the cerebral aqueduct, tectum, tegmentum, cerebral peduncles, and several cranial nerve nuclei (III and IV).

Neurites are extensions of a neuron (a type of cell in the nervous system) that can be either an axon or a dendrite. An axon is a thin, cable-like extension that carries signals away from the cell body, while a dendrite is a branching extension that receives signals from other neurons. Neurites play a crucial role in the communication between neurons and the formation of neural networks. They are involved in the transmission of electrical and chemical signals, as well as in the growth and development of the nervous system.

Neuropsychological tests are a type of psychological assessment that measures cognitive functions, such as attention, memory, language, problem-solving, and perception. These tests are used to help diagnose and understand the cognitive impact of neurological conditions, including dementia, traumatic brain injury, stroke, Parkinson's disease, and other disorders that affect the brain.

The tests are typically administered by a trained neuropsychologist and can take several hours to complete. They may involve paper-and-pencil tasks, computerized tasks, or interactive activities. The results of the tests are compared to normative data to help identify any areas of cognitive weakness or strength.

Neuropsychological testing can provide valuable information for treatment planning, rehabilitation, and assessing response to treatment. It can also be used in research to better understand the neural basis of cognition and the impact of neurological conditions on cognitive function.

Quinolinic acid is a metabolite found in the human body, produced during the metabolism of tryptophan, an essential amino acid. It is a component of the kynurenine pathway and acts as a neuroexcitatory chemical in the brain. In excessive amounts, quinolinic acid can lead to neurotoxicity, causing damage to neurons and contributing to several neurological disorders such as Huntington's disease, Alzheimer's disease, Parkinson's disease, AIDS-dementia complex, and multiple sclerosis. It also plays a role in the pathogenesis of psychiatric conditions like schizophrenia and major depressive disorder.

Cycadophyta, also known as cycads, is a division of plants that includes several species of mostly tropical and subtropical gymnosperms. These plants are characterized by a large crown of compound leaves, a stout trunk often undergrown by other plants, and a cone-like reproductive structure. Cycads are considered to be living fossils because they have remained relatively unchanged for millions of years and are thought to resemble some of the earliest seed plants. They are found in scattered locations around the world, particularly in the Americas, Africa, Asia, and the Pacific Islands. Some cycad species are endangered due to habitat loss and overcollection for ornamental purposes.

'Caenorhabditis elegans' is a species of free-living, transparent nematode (roundworm) that is widely used as a model organism in scientific research, particularly in the fields of biology and genetics. It has a simple anatomy, short lifespan, and fully sequenced genome, making it an ideal subject for studying various biological processes and diseases.

Some notable features of C. elegans include:

* Small size: Adult hermaphrodites are about 1 mm in length.
* Short lifespan: The average lifespan of C. elegans is around 2-3 weeks, although some strains can live up to 4 weeks under laboratory conditions.
* Development: C. elegans has a well-characterized developmental process, with adults developing from eggs in just 3 days at 20°C.
* Transparency: The transparent body of C. elegans allows researchers to observe its internal structures and processes easily.
* Genetics: C. elegans has a fully sequenced genome, which contains approximately 20,000 genes. Many of these genes have human homologs, making it an excellent model for studying human diseases.
* Neurobiology: C. elegans has a simple nervous system, with only 302 neurons in the hermaphrodite and 383 in the male. This simplicity makes it an ideal organism for studying neural development, function, and behavior.

Research using C. elegans has contributed significantly to our understanding of various biological processes, including cell division, apoptosis, aging, learning, and memory. Additionally, studies on C. elegans have led to the discovery of many genes associated with human diseases such as cancer, neurodegenerative disorders, and metabolic conditions.

Tertiary protein structure refers to the three-dimensional arrangement of all the elements (polypeptide chains) of a single protein molecule. It is the highest level of structural organization and results from interactions between various side chains (R groups) of the amino acids that make up the protein. These interactions, which include hydrogen bonds, ionic bonds, van der Waals forces, and disulfide bridges, give the protein its unique shape and stability, which in turn determines its function. The tertiary structure of a protein can be stabilized by various factors such as temperature, pH, and the presence of certain ions. Any changes in these factors can lead to denaturation, where the protein loses its tertiary structure and thus its function.

Stem cell transplantation is a medical procedure where stem cells, which are immature and unspecialized cells with the ability to differentiate into various specialized cell types, are introduced into a patient. The main purpose of this procedure is to restore the function of damaged or destroyed tissues or organs, particularly in conditions that affect the blood and immune systems, such as leukemia, lymphoma, aplastic anemia, and inherited metabolic disorders.

There are two primary types of stem cell transplantation: autologous and allogeneic. In autologous transplantation, the patient's own stem cells are collected, stored, and then reinfused back into their body after high-dose chemotherapy or radiation therapy to destroy the diseased cells. In allogeneic transplantation, stem cells are obtained from a donor (related or unrelated) whose human leukocyte antigen (HLA) type closely matches that of the recipient.

The process involves several steps: first, the patient undergoes conditioning therapy to suppress their immune system and make space for the new stem cells. Then, the harvested stem cells are infused into the patient's bloodstream, where they migrate to the bone marrow and begin to differentiate and produce new blood cells. This procedure requires close monitoring and supportive care to manage potential complications such as infections, graft-versus-host disease, and organ damage.

Gene expression is the process by which the information encoded in a gene is used to synthesize a functional gene product, such as a protein or RNA molecule. This process involves several steps: transcription, RNA processing, and translation. During transcription, the genetic information in DNA is copied into a complementary RNA molecule, known as messenger RNA (mRNA). The mRNA then undergoes RNA processing, which includes adding a cap and tail to the mRNA and splicing out non-coding regions called introns. The resulting mature mRNA is then translated into a protein on ribosomes in the cytoplasm through the process of translation.

The regulation of gene expression is a complex and highly controlled process that allows cells to respond to changes in their environment, such as growth factors, hormones, and stress signals. This regulation can occur at various stages of gene expression, including transcriptional activation or repression, RNA processing, mRNA stability, and translation. Dysregulation of gene expression has been implicated in many diseases, including cancer, genetic disorders, and neurological conditions.

'Drosophila proteins' refer to the proteins that are expressed in the fruit fly, Drosophila melanogaster. This organism is a widely used model system in genetics, developmental biology, and molecular biology research. The study of Drosophila proteins has contributed significantly to our understanding of various biological processes, including gene regulation, cell signaling, development, and aging.

Some examples of well-studied Drosophila proteins include:

1. HSP70 (Heat Shock Protein 70): A chaperone protein involved in protein folding and protection from stress conditions.
2. TUBULIN: A structural protein that forms microtubules, important for cell division and intracellular transport.
3. ACTIN: A cytoskeletal protein involved in muscle contraction, cell motility, and maintenance of cell shape.
4. BETA-GALACTOSIDASE (LACZ): A reporter protein often used to monitor gene expression patterns in transgenic flies.
5. ENDOGLIN: A protein involved in the development of blood vessels during embryogenesis.
6. P53: A tumor suppressor protein that plays a crucial role in preventing cancer by regulating cell growth and division.
7. JUN-KINASE (JNK): A signaling protein involved in stress response, apoptosis, and developmental processes.
8. DECAPENTAPLEGIC (DPP): A member of the TGF-β (Transforming Growth Factor Beta) superfamily, playing essential roles in embryonic development and tissue homeostasis.

These proteins are often studied using various techniques such as biochemistry, genetics, molecular biology, and structural biology to understand their functions, interactions, and regulation within the cell.

Tyrosine 3-Monooxygenase (also known as Tyrosinase or Tyrosine hydroxylase) is an enzyme that plays a crucial role in the synthesis of catecholamines, which are neurotransmitters and hormones in the body. This enzyme catalyzes the conversion of the amino acid L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by adding a hydroxyl group to the 3rd carbon atom of the tyrosine molecule.

The reaction is as follows:

L-Tyrosine + O2 + pterin (co-factor) -> L-DOPA + pterin (oxidized) + H2O

This enzyme requires molecular oxygen and a co-factor such as tetrahydrobiopterin to carry out the reaction. Tyrosine 3-Monooxygenase is found in various tissues, including the brain and adrenal glands, where it helps regulate the production of catecholamines like dopamine, norepinephrine, and epinephrine. Dysregulation of this enzyme has been implicated in several neurological disorders, such as Parkinson's disease.

Oligodendroglia are a type of neuroglial cell found in the central nervous system (CNS) of vertebrates, including humans. These cells play a crucial role in providing support and insulation to nerve fibers (axons) in the CNS, which includes the brain and spinal cord.

More specifically, oligodendroglia produce a fatty substance called myelin that wraps around axons, forming myelin sheaths. This myelination process helps to increase the speed of electrical impulse transmission (nerve impulses) along the axons, allowing for efficient communication between different neurons.

In addition to their role in myelination, oligodendroglia also contribute to the overall health and maintenance of the CNS by providing essential nutrients and supporting factors to neurons. Dysfunction or damage to oligodendroglia has been implicated in various neurological disorders, such as multiple sclerosis (MS), where demyelination of axons leads to impaired nerve function and neurodegeneration.

Primary Progressive Aphasia (PPA) is a neurological disorder characterized by progressive loss of language capabilities, while other cognitive abilities remain preserved. It is a type of dementia that primarily affects speech and language. Unlike other forms of aphasia that result from stroke or head injury, PPA is degenerative and gets worse over time.

There are three main types of PPA:

1. Semantic Variant PPA (svPPA): This type is characterized by difficulty in understanding words and objects, despite having no trouble with the mechanics of speech or writing. Over time, people with svPPA may lose their ability to understand spoken or written language, as well as to recognize objects and faces.

2. Nonfluent/Agrammatic Variant PPA (nfvPPA): This type is characterized by difficulty with speaking and writing, including producing grammatical sentences and articulating words. People with nfvPPA may also have problems with understanding spoken language, particularly when it comes to complex sentences or ambiguous phrases.

3. Logopenic Variant PPA (lvPPA): This type is characterized by difficulty with word-finding and sentence repetition, while speech remains fluent. People with lvPPA may also have problems with understanding spoken language, particularly when it comes to complex sentences or ambiguous phrases.

The exact cause of PPA is not known, but it is believed to be related to degeneration of specific areas of the brain involved in language processing, such as Broca's area and Wernicke's area. There is currently no cure for PPA, but speech and language therapy can help to slow down the progression of the disorder and improve communication skills.

Progressive Myoclonic Epilepsies (PME) is a group of rare, genetic disorders characterized by myoclonus (rapid, involuntary muscle jerks), tonic-clonic seizures (also known as grand mal seizures), and progressive neurological deterioration. The term "progressive" refers to the worsening of symptoms over time.

The myoclonic epilepsies are classified as progressive due to the underlying neurodegenerative process that affects the brain, leading to a decline in cognitive abilities, motor skills, and overall functioning. These disorders usually begin in childhood or adolescence and tend to worsen with age.

Examples of PMEs include:

1. Lafora disease: A genetic disorder caused by mutations in the EPM2A or NHLRC1 genes, leading to the accumulation of abnormal protein aggregates called Lafora bodies in neurons. Symptoms typically start between ages 6 and 16 and include myoclonus, seizures, and progressive neurological decline.
2. Unverricht-Lundborg disease: Also known as Baltic myoclonus, this is an autosomal recessive disorder caused by mutations in the CSTB gene. It is characterized by progressive myoclonic epilepsy, ataxia (loss of coordination), and cognitive decline. Symptoms usually begin between ages 6 and 18.
3. Neuronal Ceroid Lipofuscinoses (NCLs): A group of inherited neurodegenerative disorders characterized by the accumulation of lipopigments in neurons. Several types of NCLs can present with progressive myoclonic epilepsy, including CLN2 (late-infantile NCL), CLN3 (juvenile NCL), and CLN6 (early juvenile NCL).
4. Myoclonus Epilepsy Associated with Ragged Red Fibers (MERRF): A mitochondrial disorder caused by mutations in the MT-TK gene, leading to myoclonic epilepsy, ataxia, and ragged red fibers on muscle biopsy.
5. Dentatorubral-Pallidoluysian Atrophy (DRPLA): An autosomal dominant disorder caused by mutations in the ATN1 gene, characterized by myoclonic epilepsy, ataxia, chorea (involuntary movements), and dementia.

These are just a few examples of disorders that can present with progressive myoclonic epilepsy. It is essential to consult a neurologist or epileptologist for proper diagnosis and management.

In the context of medicine, iron is an essential micromineral and key component of various proteins and enzymes. It plays a crucial role in oxygen transport, DNA synthesis, and energy production within the body. Iron exists in two main forms: heme and non-heme. Heme iron is derived from hemoglobin and myoglobin in animal products, while non-heme iron comes from plant sources and supplements.

The recommended daily allowance (RDA) for iron varies depending on age, sex, and life stage:

* For men aged 19-50 years, the RDA is 8 mg/day
* For women aged 19-50 years, the RDA is 18 mg/day
* During pregnancy, the RDA increases to 27 mg/day
* During lactation, the RDA for breastfeeding mothers is 9 mg/day

Iron deficiency can lead to anemia, characterized by fatigue, weakness, and shortness of breath. Excessive iron intake may result in iron overload, causing damage to organs such as the liver and heart. Balanced iron levels are essential for maintaining optimal health.

Neurologic mutant mice are genetically engineered or spontaneously mutated rodents that are used as models to study various neurological disorders and conditions. These mice have specific genetic modifications or mutations that affect their nervous system, leading to phenotypes that resemble human neurological diseases.

Some examples of neurologic mutant mice include:

1. Alzheimer's disease models: Mice that overexpress genes associated with Alzheimer's disease, such as the amyloid precursor protein (APP) or presenilin 1 (PS1), to study the pathogenesis and potential treatments of this disorder.
2. Parkinson's disease models: Mice that have genetic mutations in genes associated with Parkinson's disease, such as alpha-synuclein or parkin, to investigate the mechanisms underlying this condition and develop new therapies.
3. Huntington's disease models: Mice that carry an expanded CAG repeat in the huntingtin gene to replicate the genetic defect seen in humans with Huntington's disease and study disease progression and treatment strategies.
4. Epilepsy models: Mice with genetic mutations that cause spontaneous seizures or increased susceptibility to seizures, used to investigate the underlying mechanisms of epilepsy and develop new treatments.
5. Stroke models: Mice that have surgical induction of stroke or genetic modifications that increase the risk of stroke, used to study the pathophysiology of stroke and identify potential therapeutic targets.

Neurologic mutant mice are essential tools in biomedical research, allowing scientists to investigate the complex interactions between genes and the environment that contribute to neurological disorders. These models help researchers better understand disease mechanisms, develop new therapies, and test their safety and efficacy before moving on to clinical trials in humans.

Neuroimmunomodulation is a complex process that refers to the interaction and communication between the nervous system (including the brain, spinal cord, and nerves) and the immune system. This interaction can have modulatory effects on both systems, influencing their functions and responses.

In simpler terms, neuroimmunomodulation describes how the nervous system and the immune system can affect each other's activities, leading to changes in behavior, inflammation, and immune response. For example, stress or depression can influence the immune system's ability to fight off infections, while an overactive immune response can lead to neurological symptoms such as fatigue, confusion, or mood changes.

Neuroimmunomodulation plays a crucial role in maintaining homeostasis and health in the body, and its dysregulation has been implicated in various diseases, including autoimmune disorders, neurodegenerative diseases, and mental health conditions. Understanding this complex interplay is essential for developing effective treatments and therapies for these conditions.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

HSP70 heat-shock proteins are a family of highly conserved molecular chaperones that play a crucial role in protein folding and protection against stress-induced damage. They are named after the fact that they were first discovered in response to heat shock, but they are now known to be produced in response to various stressors, such as oxidative stress, inflammation, and exposure to toxins.

HSP70 proteins bind to exposed hydrophobic regions of unfolded or misfolded proteins, preventing their aggregation and assisting in their proper folding. They also help target irreversibly damaged proteins for degradation by the proteasome. In addition to their role in protein homeostasis, HSP70 proteins have been shown to have anti-inflammatory and immunomodulatory effects, making them a subject of interest in various therapeutic contexts.

Neuritis is a general term that refers to inflammation of a nerve or nerves, often causing pain, loss of function, and/or sensory changes. It can affect any part of the nervous system, including the peripheral nerves (those outside the brain and spinal cord) or the cranial nerves (those that serve the head and neck). Neuritis may result from various causes, such as infections, autoimmune disorders, trauma, toxins, or metabolic conditions. The specific symptoms and treatment depend on the underlying cause and the affected nerve(s).

Transfection is a term used in molecular biology that refers to the process of deliberately introducing foreign genetic material (DNA, RNA or artificial gene constructs) into cells. This is typically done using chemical or physical methods, such as lipofection or electroporation. Transfection is widely used in research and medical settings for various purposes, including studying gene function, producing proteins, developing gene therapies, and creating genetically modified organisms. It's important to note that transfection is different from transduction, which is the process of introducing genetic material into cells using viruses as vectors.

The nervous system is a complex, highly organized network of specialized cells called neurons and glial cells that communicate with each other via electrical and chemical signals to coordinate various functions and activities in the body. It consists of two main parts: the central nervous system (CNS), including the brain and spinal cord, and the peripheral nervous system (PNS), which includes all the nerves and ganglia outside the CNS.

The primary function of the nervous system is to receive, process, and integrate information from both internal and external environments and then respond by generating appropriate motor outputs or behaviors. This involves sensing various stimuli through specialized receptors, transmitting this information through afferent neurons to the CNS for processing, integrating this information with other inputs and memories, making decisions based on this processed information, and finally executing responses through efferent neurons that control effector organs such as muscles and glands.

The nervous system can be further divided into subsystems based on their functions, including the somatic nervous system, which controls voluntary movements and reflexes; the autonomic nervous system, which regulates involuntary physiological processes like heart rate, digestion, and respiration; and the enteric nervous system, which is a specialized subset of the autonomic nervous system that controls gut functions. Overall, the nervous system plays a critical role in maintaining homeostasis, regulating behavior, and enabling cognition and consciousness.

HSP40, also known as heat shock protein 40 or DNAJ proteins, are a family of chaperone proteins that play a crucial role in the folding and assembly of other proteins. They are named after their ability to be upregulated in response to heat shock and other stress conditions that can cause protein misfolding and aggregation.

HSP40 proteins function as co-chaperones, working together with HSP70 chaperone proteins to facilitate the folding of nascent polypeptides or the refolding of denatured proteins. They contain a highly conserved J-domain that interacts with the ATPase domain of HSP70, stimulating its ATP hydrolysis activity and promoting the binding of HSP70 to client proteins.

HSP40 proteins can also play a role in protein degradation by targeting misfolded or aggregated proteins for destruction by the proteasome or autophagy pathways. Additionally, they have been implicated in various cellular processes such as transcription regulation, DNA repair, and apoptosis.

There are several subfamilies of HSP40 proteins, classified based on their structural features and functions. These include the DNAJA, DNAJB, and DNAJC subfamilies, each with distinct domains and cellular localization patterns. Dysregulation of HSP40 proteins has been linked to various diseases, including neurodegenerative disorders, cancer, and infectious diseases.

The "age of onset" is a medical term that refers to the age at which an individual first develops or displays symptoms of a particular disease, disorder, or condition. It can be used to describe various medical conditions, including both physical and mental health disorders. The age of onset can have implications for prognosis, treatment approaches, and potential causes of the condition. In some cases, early onset may indicate a more severe or progressive course of the disease, while late-onset symptoms might be associated with different underlying factors or etiologies. It is essential to provide accurate and precise information regarding the age of onset when discussing a patient's medical history and treatment plan.

Cell differentiation is the process by which a less specialized cell, or stem cell, becomes a more specialized cell type with specific functions and structures. This process involves changes in gene expression, which are regulated by various intracellular signaling pathways and transcription factors. Differentiation results in the development of distinct cell types that make up tissues and organs in multicellular organisms. It is a crucial aspect of embryonic development, tissue repair, and maintenance of homeostasis in the body.

Neuroblastoma is defined as a type of cancer that develops from immature nerve cells found in the fetal or early postnatal period, called neuroblasts. It typically occurs in infants and young children, with around 90% of cases diagnosed before age five. The tumors often originate in the adrenal glands but can also arise in the neck, chest, abdomen, or spine. Neuroblastoma is characterized by its ability to spread (metastasize) to other parts of the body, including bones, bone marrow, lymph nodes, and skin. The severity and prognosis of neuroblastoma can vary widely, depending on factors such as the patient's age at diagnosis, stage of the disease, and specific genetic features of the tumor.

"Newborn animals" refers to the very young offspring of animals that have recently been born. In medical terminology, newborns are often referred to as "neonates," and they are classified as such from birth until about 28 days of age. During this time period, newborn animals are particularly vulnerable and require close monitoring and care to ensure their survival and healthy development.

The specific needs of newborn animals can vary widely depending on the species, but generally, they require warmth, nutrition, hydration, and protection from harm. In many cases, newborns are unable to regulate their own body temperature or feed themselves, so they rely heavily on their mothers for care and support.

In medical settings, newborn animals may be examined and treated by veterinarians to ensure that they are healthy and receiving the care they need. This can include providing medical interventions such as feeding tubes, antibiotics, or other treatments as needed to address any health issues that arise. Overall, the care and support of newborn animals is an important aspect of animal medicine and conservation efforts.

Homeostasis is a fundamental concept in the field of medicine and physiology, referring to the body's ability to maintain a stable internal environment, despite changes in external conditions. It is the process by which biological systems regulate their internal environment to remain in a state of dynamic equilibrium. This is achieved through various feedback mechanisms that involve sensors, control centers, and effectors, working together to detect, interpret, and respond to disturbances in the system.

For example, the body maintains homeostasis through mechanisms such as temperature regulation (through sweating or shivering), fluid balance (through kidney function and thirst), and blood glucose levels (through insulin and glucagon secretion). When homeostasis is disrupted, it can lead to disease or dysfunction in the body.

In summary, homeostasis is the maintenance of a stable internal environment within biological systems, through various regulatory mechanisms that respond to changes in external conditions.

Thiazoles are organic compounds that contain a heterocyclic ring consisting of a nitrogen atom and a sulfur atom, along with two carbon atoms and two hydrogen atoms. They have the chemical formula C3H4NS. Thiazoles are present in various natural and synthetic substances, including some vitamins, drugs, and dyes. In the context of medicine, thiazole derivatives have been developed as pharmaceuticals for their diverse biological activities, such as anti-inflammatory, antifungal, antibacterial, and antihypertensive properties. Some well-known examples include thiazide diuretics (e.g., hydrochlorothiazide) used to treat high blood pressure and edema, and the antidiabetic drug pioglitazone.

Protein isoforms are different forms or variants of a protein that are produced from a single gene through the process of alternative splicing, where different exons (or parts of exons) are included in the mature mRNA molecule. This results in the production of multiple, slightly different proteins that share a common core structure but have distinct sequences and functions. Protein isoforms can also arise from genetic variations such as single nucleotide polymorphisms or mutations that alter the protein-coding sequence of a gene. These differences in protein sequence can affect the stability, localization, activity, or interaction partners of the protein isoform, leading to functional diversity and specialization within cells and organisms.

Secondary protein structure refers to the local spatial arrangement of amino acid chains in a protein, typically described as regular repeating patterns held together by hydrogen bonds. The two most common types of secondary structures are the alpha-helix (α-helix) and the beta-pleated sheet (β-sheet). In an α-helix, the polypeptide chain twists around itself in a helical shape, with each backbone atom forming a hydrogen bond with the fourth amino acid residue along the chain. This forms a rigid rod-like structure that is resistant to bending or twisting forces. In β-sheets, adjacent segments of the polypeptide chain run parallel or antiparallel to each other and are connected by hydrogen bonds, forming a pleated sheet-like arrangement. These secondary structures provide the foundation for the formation of tertiary and quaternary protein structures, which determine the overall three-dimensional shape and function of the protein.

Maze learning is not a medical term per se, but it is a concept that is often used in the field of neuroscience and psychology. It refers to the process by which an animal or human learns to navigate through a complex environment, such as a maze, in order to find its way to a goal or target.

Maze learning involves several cognitive processes, including spatial memory, learning, and problem-solving. As animals or humans navigate through the maze, they encode information about the location of the goal and the various landmarks within the environment. This information is then used to form a cognitive map that allows them to navigate more efficiently in subsequent trials.

Maze learning has been widely used as a tool for studying learning and memory processes in both animals and humans. For example, researchers may use maze learning tasks to investigate the effects of brain damage or disease on cognitive function, or to evaluate the efficacy of various drugs or interventions for improving cognitive performance.

REM Sleep Behavior Disorder (RBD) is a parasomnia, which is a disorder that involves undesirable experiences or abnormal behaviors during sleep. Specifically, RBD is a type of rapid eye movement (REM) sleep parasomnia where the muscle atonia (lack of muscle tone) that normally occurs during REM sleep is absent or incomplete, allowing for the emergence of motor behaviors and vivid dreaming. These dreams can be quite intense and may result in the individual physically acting out their dreams, leading to potential harm for themselves or their bed partner. RBD can occur in isolation or as a symptom of another neurological condition.

Caspase-3 is a type of protease enzyme that plays a central role in the execution-phase of cell apoptosis, or programmed cell death. It's also known as CPP32 (CPP for ced-3 protease precursor) or apopain. Caspase-3 is produced as an inactive protein that is activated when cleaved by other caspases during the early stages of apoptosis. Once activated, it cleaves a variety of cellular proteins, including structural proteins, enzymes, and signal transduction proteins, leading to the characteristic morphological and biochemical changes associated with apoptotic cell death. Caspase-3 is often referred to as the "death protease" because of its crucial role in executing the cell death program.

Up-regulation is a term used in molecular biology and medicine to describe an increase in the expression or activity of a gene, protein, or receptor in response to a stimulus. This can occur through various mechanisms such as increased transcription, translation, or reduced degradation of the molecule. Up-regulation can have important functional consequences, for example, enhancing the sensitivity or response of a cell to a hormone, neurotransmitter, or drug. It is a normal physiological process that can also be induced by disease or pharmacological interventions.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Survival of Motor Neuron 1 (SMN1) protein is a critical component for the survival of motor neurons, which are nerve cells that control muscle movements. The SMN1 protein is produced by the Survival of Motor Neuron 1 gene, located on human chromosome 5q13.

The primary function of the SMN1 protein is to assist in the biogenesis of small nuclear ribonucleoproteins (snRNPs), which are essential for spliceosomes - complex molecular machines responsible for RNA processing in the cell. The absence or significant reduction of SMN1 protein leads to defective snRNP assembly, impaired RNA splicing, and ultimately results in motor neuron degeneration.

Mutations in the SMN1 gene can cause Spinal Muscular Atrophy (SMA), a genetic disorder characterized by progressive muscle weakness, atrophy, and paralysis due to the loss of lower motor neurons in the spinal cord. The severity of SMA depends on the amount of functional SMN1 protein produced, with less protein leading to more severe symptoms.

Molecular models are three-dimensional representations of molecular structures that are used in the field of molecular biology and chemistry to visualize and understand the spatial arrangement of atoms and bonds within a molecule. These models can be physical or computer-generated and allow researchers to study the shape, size, and behavior of molecules, which is crucial for understanding their function and interactions with other molecules.

Physical molecular models are often made up of balls (representing atoms) connected by rods or sticks (representing bonds). These models can be constructed manually using materials such as plastic or wooden balls and rods, or they can be created using 3D printing technology.

Computer-generated molecular models, on the other hand, are created using specialized software that allows researchers to visualize and manipulate molecular structures in three dimensions. These models can be used to simulate molecular interactions, predict molecular behavior, and design new drugs or chemicals with specific properties. Overall, molecular models play a critical role in advancing our understanding of molecular structures and their functions.

Single-stranded DNA breaks (SSBs) refer to a type of DNA damage in which one strand of the double-helix structure is cleaved or broken. This kind of damage can occur spontaneously due to cellular metabolism or can be induced by various genotoxic agents, such as ionizing radiation and certain chemicals.

SSBs are typically repaired rapidly and efficiently by enzymes known as DNA repair proteins. However, if left unrepaired or misrepaired, they can lead to mutations, genomic instability, and increased risk of diseases, including cancer. In some cases, single-stranded breaks may also precede the formation of more severe double-stranded DNA breaks (DSBs).

It is important to note that while SSBs are less catastrophic than DSBs, they still play a significant role in genome maintenance and cellular health.

According to the National Institutes of Health (NIH), stem cells are "initial cells" or "precursor cells" that have the ability to differentiate into many different cell types in the body. They can also divide without limit to replenish other cells for as long as the person or animal is still alive.

There are two main types of stem cells: embryonic stem cells, which come from human embryos, and adult stem cells, which are found in various tissues throughout the body. Embryonic stem cells have the ability to differentiate into all cell types in the body, while adult stem cells have more limited differentiation potential.

Stem cells play an essential role in the development and repair of various tissues and organs in the body. They are currently being studied for their potential use in the treatment of a wide range of diseases and conditions, including cancer, diabetes, heart disease, and neurological disorders. However, more research is needed to fully understand the properties and capabilities of these cells before they can be used safely and effectively in clinical settings.

Glycogen Synthase Kinase 3 (GSK-3) is a serine/threonine protein kinase that plays a crucial role in the regulation of several cellular processes, including glycogen metabolism, cell signaling, gene transcription, and apoptosis. It was initially discovered as a key enzyme involved in glycogen metabolism due to its ability to phosphorylate and inhibit glycogen synthase, an enzyme responsible for the synthesis of glycogen from glucose.

GSK-3 exists in two isoforms, GSK-3α and GSK-3β, which share a high degree of sequence similarity and are widely expressed in various tissues. Both isoforms are constitutively active under normal conditions and are regulated through inhibitory phosphorylation by several upstream signaling pathways, such as insulin, Wnt, and Hedgehog signaling.

Dysregulation of GSK-3 has been implicated in the pathogenesis of various diseases, including diabetes, neurodegenerative disorders, and cancer. In recent years, GSK-3 has emerged as an attractive therapeutic target for the development of novel drugs to treat these conditions.

Nerve Growth Factors (NGFs) are a family of proteins that play an essential role in the growth, maintenance, and survival of certain neurons (nerve cells). They were first discovered by Rita Levi-Montalcini and Stanley Cohen in 1956. NGF is particularly crucial for the development and function of the peripheral nervous system, which connects the central nervous system to various organs and tissues throughout the body.

NGF supports the differentiation and survival of sympathetic and sensory neurons during embryonic development. In adults, NGF continues to regulate the maintenance and repair of these neurons, contributing to neuroplasticity – the brain's ability to adapt and change over time. Additionally, NGF has been implicated in pain transmission and modulation, as well as inflammatory responses.

Abnormal levels or dysfunctional NGF signaling have been associated with various medical conditions, including neurodegenerative diseases (e.g., Alzheimer's and Parkinson's), chronic pain disorders, and certain cancers (e.g., small cell lung cancer). Therefore, understanding the role of NGF in physiological and pathological processes may provide valuable insights into developing novel therapeutic strategies for these conditions.

Memory disorders are a category of cognitive impairments that affect an individual's ability to acquire, store, retain, and retrieve memories. These disorders can be caused by various underlying medical conditions, including neurological disorders, psychiatric illnesses, substance abuse, or even normal aging processes. Some common memory disorders include:

1. Alzheimer's disease: A progressive neurodegenerative disorder that primarily affects older adults and is characterized by a decline in cognitive abilities, including memory, language, problem-solving, and decision-making skills.
2. Dementia: A broader term used to describe a group of symptoms associated with a decline in cognitive function severe enough to interfere with daily life. Alzheimer's disease is the most common cause of dementia, but other causes include vascular dementia, Lewy body dementia, and frontotemporal dementia.
3. Amnesia: A memory disorder characterized by difficulties in forming new memories or recalling previously learned information due to brain damage or disease. Amnesia can be temporary or permanent and may result from head trauma, stroke, infection, or substance abuse.
4. Mild cognitive impairment (MCI): A condition where an individual experiences mild but noticeable memory or cognitive difficulties that are greater than expected for their age and education level. While some individuals with MCI may progress to dementia, others may remain stable or even improve over time.
5. Korsakoff's syndrome: A memory disorder often caused by alcohol abuse and thiamine deficiency, characterized by severe short-term memory loss, confabulation (making up stories to fill in memory gaps), and disorientation.

It is essential to consult a healthcare professional if you or someone you know experiences persistent memory difficulties, as early diagnosis and intervention can help manage symptoms and improve quality of life.

Nuclear factor erythroid-derived 2-like 2 (NFE2L2), also known as NF-E2-related factor 2 (NRF2), is a protein that plays a crucial role in the regulation of cellular responses to oxidative stress and electrophilic substances. It is a transcription factor that binds to the antioxidant response element (ARE) in the promoter region of various genes, inducing their expression and promoting cellular defense against harmful stimuli.

Under normal conditions, NRF2 is bound to its inhibitor, Kelch-like ECH-associated protein 1 (KEAP1), in the cytoplasm, where it is targeted for degradation by the proteasome. However, upon exposure to oxidative stress or electrophilic substances, KEAP1 undergoes conformational changes, leading to the release and stabilization of NRF2. Subsequently, NRF2 translocates to the nucleus, forms a complex with small Maf proteins, and binds to AREs, inducing the expression of genes involved in antioxidant response, detoxification, and cellular protection.

Genetic variations or dysregulation of the NFE2L2/KEAP1 pathway have been implicated in several diseases, including cancer, neurodegenerative disorders, and pulmonary fibrosis, highlighting its importance in maintaining cellular homeostasis and preventing disease progression.

Multiple Sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. In MS, the immune system mistakenly attacks the protective covering of nerve fibers, called myelin, leading to damage and scarring (sclerosis). This results in disrupted communication between the brain and the rest of the body, causing a variety of neurological symptoms that can vary widely from person to person.

The term "multiple" refers to the numerous areas of scarring that occur throughout the CNS in this condition. The progression, severity, and specific symptoms of MS are unpredictable and may include vision problems, muscle weakness, numbness or tingling, difficulty with balance and coordination, cognitive impairment, and mood changes. There is currently no cure for MS, but various treatments can help manage symptoms, modify the course of the disease, and improve quality of life for those affected.

Apraxia is a motor disorder characterized by the inability to perform learned, purposeful movements despite having the physical ability and mental understanding to do so. It is not caused by weakness, paralysis, or sensory loss, and it is not due to poor comprehension or motivation.

There are several types of apraxias, including:

1. Limb-Kinematic Apraxia: This type affects the ability to make precise movements with the limbs, such as using tools or performing complex gestures.
2. Ideomotor Apraxia: In this form, individuals have difficulty executing learned motor actions in response to verbal commands or visual cues, but they can still perform the same action when given the actual object to use.
3. Ideational Apraxia: This type affects the ability to sequence and coordinate multiple steps of a complex action, such as dressing oneself or making coffee.
4. Oral Apraxia: Also known as verbal apraxia, this form affects the ability to plan and execute speech movements, leading to difficulties with articulation and speech production.
5. Constructional Apraxia: This type impairs the ability to draw, copy, or construct geometric forms and shapes, often due to visuospatial processing issues.

Apraxias can result from various neurological conditions, such as stroke, brain injury, dementia, or neurodegenerative diseases like Parkinson's disease and Alzheimer's disease. Treatment typically involves rehabilitation and therapy focused on retraining the affected movements and compensating for any residual deficits.

Neuroimaging is a medical term that refers to the use of various techniques to either directly or indirectly image the structure, function, or pharmacology of the nervous system. It includes techniques such as computed tomography (CT), magnetic resonance imaging (MRI), functional MRI (fMRI), positron emission tomography (PET), single-photon emission computed tomography (SPECT), and diffusion tensor imaging (DTI). These techniques are used to diagnose and monitor various neurological and psychiatric conditions, as well as to understand the underlying mechanisms of brain function in health and disease.

Heat-shock proteins (HSPs) are a group of conserved proteins that are produced by cells in response to stressful conditions, such as increased temperature, exposure to toxins, or infection. They play an essential role in protecting cells and promoting their survival under stressful conditions by assisting in the proper folding and assembly of other proteins, preventing protein aggregation, and helping to refold or degrade damaged proteins. HSPs are named according to their molecular weight, for example, HSP70 and HSP90. They are found in all living organisms, from bacteria to humans, indicating their fundamental importance in cellular function and survival.

Protein conformation refers to the specific three-dimensional shape that a protein molecule assumes due to the spatial arrangement of its constituent amino acid residues and their associated chemical groups. This complex structure is determined by several factors, including covalent bonds (disulfide bridges), hydrogen bonds, van der Waals forces, and ionic bonds, which help stabilize the protein's unique conformation.

Protein conformations can be broadly classified into two categories: primary, secondary, tertiary, and quaternary structures. The primary structure represents the linear sequence of amino acids in a polypeptide chain. The secondary structure arises from local interactions between adjacent amino acid residues, leading to the formation of recurring motifs such as α-helices and β-sheets. Tertiary structure refers to the overall three-dimensional folding pattern of a single polypeptide chain, while quaternary structure describes the spatial arrangement of multiple folded polypeptide chains (subunits) that interact to form a functional protein complex.

Understanding protein conformation is crucial for elucidating protein function, as the specific three-dimensional shape of a protein directly influences its ability to interact with other molecules, such as ligands, nucleic acids, or other proteins. Any alterations in protein conformation due to genetic mutations, environmental factors, or chemical modifications can lead to loss of function, misfolding, aggregation, and disease states like neurodegenerative disorders and cancer.

In the context of medical and clinical neuroscience, memory is defined as the brain's ability to encode, store, retain, and recall information or experiences. Memory is a complex cognitive process that involves several interconnected regions of the brain and can be categorized into different types based on various factors such as duration and the nature of the information being remembered.

The major types of memory include:

1. Sensory memory: The shortest form of memory, responsible for holding incoming sensory information for a brief period (less than a second to several seconds) before it is either transferred to short-term memory or discarded.
2. Short-term memory (also called working memory): A temporary storage system that allows the brain to hold and manipulate information for approximately 20-30 seconds, although this duration can be extended through rehearsal strategies. Short-term memory has a limited capacity, typically thought to be around 7±2 items.
3. Long-term memory: The memory system responsible for storing large amounts of information over extended periods, ranging from minutes to a lifetime. Long-term memory has a much larger capacity compared to short-term memory and is divided into two main categories: explicit (declarative) memory and implicit (non-declarative) memory.

Explicit (declarative) memory can be further divided into episodic memory, which involves the recollection of specific events or episodes, including their temporal and spatial contexts, and semantic memory, which refers to the storage and retrieval of general knowledge, facts, concepts, and vocabulary, independent of personal experience or context.

Implicit (non-declarative) memory encompasses various forms of learning that do not require conscious awareness or intention, such as procedural memory (skills and habits), priming (facilitated processing of related stimuli), classical conditioning (associative learning), and habituation (reduced responsiveness to repeated stimuli).

Memory is a crucial aspect of human cognition and plays a significant role in various aspects of daily life, including learning, problem-solving, decision-making, social interactions, and personal identity. Memory dysfunction can result from various neurological and psychiatric conditions, such as dementia, Alzheimer's disease, stroke, traumatic brain injury, and depression.

Hydrogen peroxide (H2O2) is a colorless, odorless, clear liquid with a slightly sweet taste, although drinking it is harmful and can cause poisoning. It is a weak oxidizing agent and is used as an antiseptic and a bleaching agent. In diluted form, it is used to disinfect wounds and kill bacteria and viruses on the skin; in higher concentrations, it can be used to bleach hair or remove stains from clothing. It is also used as a propellant in rocketry and in certain industrial processes. Chemically, hydrogen peroxide is composed of two hydrogen atoms and two oxygen atoms, and it is structurally similar to water (H2O), with an extra oxygen atom. This gives it its oxidizing properties, as the additional oxygen can be released and used to react with other substances.

Presenilin-1 (PSEN1) is a gene that provides instructions for making one part of an enzyme complex called gamma-secretase. This enzyme is involved in the breakdown of certain proteins, most notably the amyloid precursor protein (APP), into smaller fragments called peptides. One of these peptides, called beta-amyloid, can accumulate and form clumps called plaques, which are a characteristic feature of Alzheimer's disease.

Mutations in the PSEN1 gene have been identified as a major cause of early-onset familial Alzheimer's disease (FAD), a rare, inherited form of the disorder that usually develops before age 65. These mutations result in an abnormal gamma-secretase enzyme that produces more toxic beta-amyloid peptides and fewer harmless ones, leading to the formation of amyloid plaques and neurodegeneration.

It's important to note that while mutations in PSEN1 are associated with early-onset FAD, most cases of Alzheimer's disease are sporadic and develop later in life, typically after age 65. The role of PSEN1 and other genes associated with FAD in the more common, late-onset form of Alzheimer's is still being researched.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Dipeptidyl-peptidases (DPPs) and tripeptidyl-peptidases (TPPs) are two types of enzymes that belong to the class of peptidases, which are proteins that help break down other proteins into smaller peptides or individual amino acids.

Dipeptidyl-peptidases cleave dipeptides (two-amino acid units) from the N-terminus (the end with a free amino group) of polypeptides and proteins, while tripeptidyl-peptidases cleave tripeptides (three-amino acid units) from the same location.

There are several different isoforms of DPPs and TPPs that have been identified in various organisms, including humans. These enzymes play important roles in regulating various physiological processes, such as digestion, immune function, and blood glucose homeostasis.

Inhibitors of DPP-4, one specific isoform of DPPs, have been developed for the treatment of type 2 diabetes, as they help increase the levels of incretin hormones that stimulate insulin secretion and suppress glucagon production.

Membrane proteins are a type of protein that are embedded in the lipid bilayer of biological membranes, such as the plasma membrane of cells or the inner membrane of mitochondria. These proteins play crucial roles in various cellular processes, including:

1. Cell-cell recognition and signaling
2. Transport of molecules across the membrane (selective permeability)
3. Enzymatic reactions at the membrane surface
4. Energy transduction and conversion
5. Mechanosensation and signal transduction

Membrane proteins can be classified into two main categories: integral membrane proteins, which are permanently associated with the lipid bilayer, and peripheral membrane proteins, which are temporarily or loosely attached to the membrane surface. Integral membrane proteins can further be divided into three subcategories based on their topology:

1. Transmembrane proteins, which span the entire width of the lipid bilayer with one or more alpha-helices or beta-barrels.
2. Lipid-anchored proteins, which are covalently attached to lipids in the membrane via a glycosylphosphatidylinositol (GPI) anchor or other lipid modifications.
3. Monotopic proteins, which are partially embedded in the membrane and have one or more domains exposed to either side of the bilayer.

Membrane proteins are essential for maintaining cellular homeostasis and are targets for various therapeutic interventions, including drug development and gene therapy. However, their structural complexity and hydrophobicity make them challenging to study using traditional biochemical methods, requiring specialized techniques such as X-ray crystallography, nuclear magnetic resonance (NMR) spectroscopy, and single-particle cryo-electron microscopy (cryo-EM).

Paraquat is a highly toxic herbicide that is used for controlling weeds and grasses in agricultural settings. It is a non-selective contact weed killer, meaning it kills any green plant it comes into contact with. Paraquat is a fast-acting chemical that causes rapid desiccation of plant tissues upon contact.

In a medical context, paraquat is classified as a toxicological emergency and can cause severe poisoning in humans if ingested, inhaled, or comes into contact with the skin or eyes. Paraquat poisoning can lead to multiple organ failure, including the lungs, kidneys, and liver, and can be fatal in severe cases. There is no specific antidote for paraquat poisoning, and treatment typically focuses on supportive care and managing symptoms.

It's important to note that paraquat is highly regulated and its use is restricted to licensed professionals due to its high toxicity. Proper protective equipment, including gloves, goggles, and respiratory protection, should be used when handling paraquat to minimize the risk of exposure.

Fluorescence microscopy is a type of microscopy that uses fluorescent dyes or proteins to highlight and visualize specific components within a sample. In this technique, the sample is illuminated with high-energy light, typically ultraviolet (UV) or blue light, which excites the fluorescent molecules causing them to emit lower-energy, longer-wavelength light, usually visible light in the form of various colors. This emitted light is then collected by the microscope and detected to produce an image.

Fluorescence microscopy has several advantages over traditional brightfield microscopy, including the ability to visualize specific structures or molecules within a complex sample, increased sensitivity, and the potential for quantitative analysis. It is widely used in various fields of biology and medicine, such as cell biology, neuroscience, and pathology, to study the structure, function, and interactions of cells and proteins.

There are several types of fluorescence microscopy techniques, including widefield fluorescence microscopy, confocal microscopy, two-photon microscopy, and total internal reflection fluorescence (TIRF) microscopy, each with its own strengths and limitations. These techniques can provide valuable insights into the behavior of cells and proteins in health and disease.

The neostriatum is a component of the basal ganglia, a group of subcortical nuclei in the brain that are involved in motor control, procedural learning, and other cognitive functions. It is composed primarily of two types of neurons: medium spiny neurons and aspiny interneurons. The neostriatum receives input from various regions of the cerebral cortex and projects to other parts of the basal ganglia, forming an important part of the cortico-basal ganglia-thalamo-cortical loop.

In medical terminology, the neostriatum is often used interchangeably with the term "striatum," although some sources reserve the term "neostriatum" for the caudate nucleus and putamen specifically, while using "striatum" to refer to the entire structure including the ventral striatum (also known as the nucleus accumbens).

Damage to the neostriatum has been implicated in various neurological conditions, such as Huntington's disease and Parkinson's disease.

The endoplasmic reticulum (ER) is a network of interconnected tubules and sacs that are present in the cytoplasm of eukaryotic cells. It is a continuous membranous organelle that plays a crucial role in the synthesis, folding, modification, and transport of proteins and lipids.

The ER has two main types: rough endoplasmic reticulum (RER) and smooth endoplasmic reticulum (SER). RER is covered with ribosomes, which give it a rough appearance, and is responsible for protein synthesis. On the other hand, SER lacks ribosomes and is involved in lipid synthesis, drug detoxification, calcium homeostasis, and steroid hormone production.

In summary, the endoplasmic reticulum is a vital organelle that functions in various cellular processes, including protein and lipid metabolism, calcium regulation, and detoxification.

Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) is a laboratory technique used in molecular biology to amplify and detect specific DNA sequences. This technique is particularly useful for the detection and quantification of RNA viruses, as well as for the analysis of gene expression.

The process involves two main steps: reverse transcription and polymerase chain reaction (PCR). In the first step, reverse transcriptase enzyme is used to convert RNA into complementary DNA (cDNA) by reading the template provided by the RNA molecule. This cDNA then serves as a template for the PCR amplification step.

In the second step, the PCR reaction uses two primers that flank the target DNA sequence and a thermostable polymerase enzyme to repeatedly copy the targeted cDNA sequence. The reaction mixture is heated and cooled in cycles, allowing the primers to anneal to the template, and the polymerase to extend the new strand. This results in exponential amplification of the target DNA sequence, making it possible to detect even small amounts of RNA or cDNA.

RT-PCR is a sensitive and specific technique that has many applications in medical research and diagnostics, including the detection of viruses such as HIV, hepatitis C virus, and SARS-CoV-2 (the virus that causes COVID-19). It can also be used to study gene expression, identify genetic mutations, and diagnose genetic disorders.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Post-translational protein processing refers to the modifications and changes that proteins undergo after their synthesis on ribosomes, which are complex molecular machines responsible for protein synthesis. These modifications occur through various biochemical processes and play a crucial role in determining the final structure, function, and stability of the protein.

The process begins with the translation of messenger RNA (mRNA) into a linear polypeptide chain, which is then subjected to several post-translational modifications. These modifications can include:

1. Proteolytic cleavage: The removal of specific segments or domains from the polypeptide chain by proteases, resulting in the formation of mature, functional protein subunits.
2. Chemical modifications: Addition or modification of chemical groups to the side chains of amino acids, such as phosphorylation (addition of a phosphate group), glycosylation (addition of sugar moieties), methylation (addition of a methyl group), acetylation (addition of an acetyl group), and ubiquitination (addition of a ubiquitin protein).
3. Disulfide bond formation: The oxidation of specific cysteine residues within the polypeptide chain, leading to the formation of disulfide bonds between them. This process helps stabilize the three-dimensional structure of proteins, particularly in extracellular environments.
4. Folding and assembly: The acquisition of a specific three-dimensional conformation by the polypeptide chain, which is essential for its function. Chaperone proteins assist in this process to ensure proper folding and prevent aggregation.
5. Protein targeting: The directed transport of proteins to their appropriate cellular locations, such as the nucleus, mitochondria, endoplasmic reticulum, or plasma membrane. This is often facilitated by specific signal sequences within the protein that are recognized and bound by transport machinery.

Collectively, these post-translational modifications contribute to the functional diversity of proteins in living organisms, allowing them to perform a wide range of cellular processes, including signaling, catalysis, regulation, and structural support.

N-Methyl-D-Aspartate (NMDA) receptors are a type of ionotropic glutamate receptor, which are found in the membranes of excitatory neurons in the central nervous system. They play a crucial role in synaptic plasticity, learning, and memory processes. NMDA receptors are ligand-gated channels that are permeable to calcium ions (Ca2+) and other cations.

NMDA receptors are composed of four subunits, which can be a combination of NR1, NR2A-D, and NR3A-B subunits. The binding of the neurotransmitter glutamate to the NR2 subunit and glycine to the NR1 subunit leads to the opening of the ion channel and the influx of Ca2+ ions.

NMDA receptors have a unique property in that they require both agonist binding and membrane depolarization for full activation, making them sensitive to changes in the electrical activity of the neuron. This property allows NMDA receptors to act as coincidence detectors, playing a critical role in synaptic plasticity and learning.

Abnormal functioning of NMDA receptors has been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and chronic pain. Therefore, NMDA receptors are a common target for drug development in the treatment of these conditions.

Confocal microscopy is a powerful imaging technique used in medical and biological research to obtain high-resolution, contrast-rich images of thick samples. This super-resolution technology provides detailed visualization of cellular structures and processes at various depths within a specimen.

In confocal microscopy, a laser beam focused through a pinhole illuminates a small spot within the sample. The emitted fluorescence or reflected light from this spot is then collected by a detector, passing through a second pinhole that ensures only light from the focal plane reaches the detector. This process eliminates out-of-focus light, resulting in sharp images with improved contrast compared to conventional widefield microscopy.

By scanning the laser beam across the sample in a raster pattern and collecting fluorescence at each point, confocal microscopy generates optical sections of the specimen. These sections can be combined to create three-dimensional reconstructions, allowing researchers to study cellular architecture and interactions within complex tissues.

Confocal microscopy has numerous applications in medical research, including studying protein localization, tracking intracellular dynamics, analyzing cell morphology, and investigating disease mechanisms at the cellular level. Additionally, it is widely used in clinical settings for diagnostic purposes, such as analyzing skin lesions or detecting pathogens in patient samples.

Cycasin is a chemical compound that is found in the seeds of cycad plants. Its chemical name is methylazoxymethanol beta-D-glucoside. It is known to be toxic and carcinogenic (cancer-causing) in animals, including humans. Cycasin itself is not highly toxic, but when it is metabolized in the body, it releases a toxic compound called methylazoxymethanol. This compound can damage DNA and cause mutations, leading to cancer.

Exposure to cycasin can occur through ingestion of cycad seeds or plants that contain the compound. In some parts of the world, cycad seeds have been used as a food source, but they must be properly prepared to remove the toxic compounds. Cycasin has also been implicated in cases of poisoning in animals that have eaten contaminated feed or browsed on cycad plants.

It is important to note that cycasin is not found in significant quantities in commercially available foods or products, and exposure to this compound is relatively rare. However, it is a well-studied toxicant and carcinogen, and research into its effects continues to provide valuable insights into the mechanisms of toxicity and cancer development.

I'm sorry for any confusion, but "Ubiquitin Thiolesterase" is not a widely recognized medical term or a well-defined concept in the field of medicine. Ubiquitination, however, is a post-translational modification that plays a crucial role in various cellular processes, including protein degradation and regulation of signaling pathways.

Ubiquitin Thiolesterase could potentially refer to an enzyme that catalyzes the hydrolysis of a thioester bond between ubiquitin and a target protein. This process would be part of the ubiquitination cascade, where ubiquitin is transferred from one protein to another through various intermediates, including thioester bonds. However, I would recommend consulting primary literature or speaking with an expert in the field for more precise information on this topic.

Nerve Growth Factor (NGF) is a small secreted protein that is involved in the growth, maintenance, and survival of certain neurons (nerve cells). It was the first neurotrophin to be discovered and is essential for the development and function of the nervous system. NGF binds to specific receptors on the surface of nerve cells and helps to promote their differentiation, axonal growth, and synaptic plasticity. Additionally, NGF has been implicated in various physiological processes such as inflammation, immune response, and wound healing. Deficiencies or excesses of NGF have been linked to several neurological disorders, including Alzheimer's disease, Parkinson's disease, and pain conditions.

Adrenoleukodystrophy (ADL) is a rare genetic disorder that affects the nervous system and adrenal glands. It is characterized by the accumulation of very long-chain fatty acids (VLCFAs) in the brain, leading to progressive neurological symptoms such as behavioral changes, visual loss, hearing loss, seizures, and difficulties with coordination and movement.

ADL is caused by mutations in the ABCD1 gene, which provides instructions for making a protein involved in the breakdown of VLCFA. Without this protein, VLCFAs accumulate in the brain and adrenal glands, leading to damage and dysfunction.

There are several forms of ADL, including:

* Childhood cerebral ADL: This is the most severe form of the disorder, typically affecting boys between the ages of 4 and 8. It progresses rapidly and can lead to significant neurological impairment within a few years.
* Adrenomyeloneuropathy (AMN): This form of ADL affects both men and women and is characterized by progressive stiffness, weakness, and spasticity in the legs. It typically develops in adulthood and progresses slowly over many years.
* Addison's disease: This is a condition that affects the adrenal glands, leading to hormonal imbalances and symptoms such as fatigue, weight loss, and low blood pressure.

There is no cure for ADL, but treatments can help manage the symptoms and slow down the progression of the disorder. These may include dietary changes, medications to control seizures or hormone levels, and physical therapy. In some cases, stem cell transplantation may be recommended as a treatment option.

Brain tissue transplantation is a medical procedure that involves the surgical implantation of healthy brain tissue into a damaged or diseased brain. The goal of this procedure is to replace the non-functioning brain cells with healthy ones, in order to restore lost function or improve neurological symptoms.

The brain tissue used for transplantation can come from various sources, including fetal brain tissue, embryonic stem cells, or autologous cells (the patient's own cells). The most common type of brain tissue transplantation is fetal brain tissue transplantation, where tissue from aborted fetuses is used.

Brain tissue transplantation has been explored as a potential treatment for various neurological conditions, including Parkinson's disease, Huntington's disease, and stroke. However, the procedure remains highly experimental and is not widely available outside of clinical trials. There are also ethical concerns surrounding the use of fetal brain tissue, which has limited its widespread adoption.

It is important to note that while brain tissue transplantation holds promise as a potential treatment for neurological disorders, it is still an area of active research and much more needs to be learned about its safety and efficacy before it becomes a standard treatment option.

The intracellular space refers to the interior of a cell, specifically the area enclosed by the plasma membrane that is occupied by organelles, cytoplasm, and other cellular structures. It excludes the extracellular space, which is the area outside the cell surrounded by the plasma membrane. The intracellular space is where various metabolic processes, such as protein synthesis, energy production, and waste removal, occur. It is essential for maintaining the cell's structure, function, and survival.

Propionates, in a medical context, most commonly refer to a group of medications that are used as topical creams or gels to treat fungal infections of the skin. Propionic acid and its salts, such as propionate, are the active ingredients in these medications. They work by inhibiting the growth of fungi, which causes the infection. Common examples of propionate-containing medications include creams used to treat athlete's foot, ringworm, and jock itch.

It is important to note that there are many different types of medications and compounds that contain the word "propionate" in their name, as it refers to a specific chemical structure. However, in a medical context, it most commonly refers to antifungal creams or gels.

Retinal Ganglion Cells (RGCs) are a type of neuron located in the innermost layer of the retina, the light-sensitive tissue at the back of the eye. These cells receive visual information from photoreceptors (rods and cones) via intermediate cells called bipolar cells. RGCs then send this visual information through their long axons to form the optic nerve, which transmits the signals to the brain for processing and interpretation as vision.

There are several types of RGCs, each with distinct morphological and functional characteristics. Some RGCs are specialized in detecting specific features of the visual scene, such as motion, contrast, color, or brightness. The diversity of RGCs allows for a rich and complex representation of the visual world in the brain.

Damage to RGCs can lead to various visual impairments, including loss of vision, reduced visual acuity, and altered visual fields. Conditions associated with RGC damage or degeneration include glaucoma, optic neuritis, ischemic optic neuropathy, and some inherited retinal diseases.

Medical definitions of "oxidants" refer to them as oxidizing agents or substances that can gain electrons and be reduced. They are capable of accepting electrons from other molecules in chemical reactions, leading to the production of oxidation products. In biological systems, oxidants play a crucial role in various cellular processes such as energy production and immune responses. However, an imbalance between oxidant and antioxidant levels can lead to a state of oxidative stress, which has been linked to several diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. Examples of oxidants include reactive oxygen species (ROS), such as superoxide anion, hydrogen peroxide, and hydroxyl radical, as well as reactive nitrogen species (RNS), such as nitric oxide and peroxynitrite.

Assertiveness is a communication style that strikes a balance between being aggressive and being passive. According to the American Psychological Association (APA), assertive individuals express their thoughts, feelings, and needs in a direct, honest, and appropriate way, while also considering the rights and needs of others. This approach to communication can help individuals build and maintain positive relationships, reduce stress and anxiety, and increase self-esteem and confidence.

Being assertive involves using "I" statements to express your thoughts and feelings, rather than blaming or criticizing others. It also involves active listening, respect for others' viewpoints, and the ability to compromise when necessary. Assertiveness is not about dominating or controlling others, but rather about standing up for oneself in a way that is respectful and appropriate.

It's important to note that assertiveness may look different for different people, as it depends on individual personality traits, cultural background, and life experiences. However, with practice and support, anyone can develop assertive communication skills.

COS cells are a type of cell line that are commonly used in molecular biology and genetic research. The name "COS" is an acronym for "CV-1 in Origin," as these cells were originally derived from the African green monkey kidney cell line CV-1. COS cells have been modified through genetic engineering to express high levels of a protein called SV40 large T antigen, which allows them to efficiently take up and replicate exogenous DNA.

There are several different types of COS cells that are commonly used in research, including COS-1, COS-3, and COS-7 cells. These cells are widely used for the production of recombinant proteins, as well as for studies of gene expression, protein localization, and signal transduction.

It is important to note that while COS cells have been a valuable tool in scientific research, they are not without their limitations. For example, because they are derived from monkey kidney cells, there may be differences in the way that human genes are expressed or regulated in these cells compared to human cells. Additionally, because COS cells express SV40 large T antigen, they may have altered cell cycle regulation and other phenotypic changes that could affect experimental results. Therefore, it is important to carefully consider the choice of cell line when designing experiments and interpreting results.

Longevity, in a medical context, refers to the condition of living for a long period of time. It is often used to describe individuals who have reached a advanced age, such as 85 years or older, and is sometimes associated with the study of aging and factors that contribute to a longer lifespan.

It's important to note that longevity can be influenced by various genetic and environmental factors, including family history, lifestyle choices, and access to quality healthcare. Some researchers are also studying the potential impact of certain medical interventions, such as stem cell therapies and caloric restriction, on lifespan and healthy aging.

Nicotinamide-nucleotide adenylyltransferase (NNAT) is an enzyme that plays a crucial role in the metabolism of nicotinamide adenine dinucleotide (NAD+), which is a coenzyme involved in various redox reactions in the body. NNAT catalyzes the interconversion between nicotinamide mononucleotide (NMN) and NAD+ through the transfer of an adenylyl group.

The reaction catalyzed by NNAT is as follows:

NMN + ATP → NAD+ + PP\_i

NNAT is found in various tissues, including the brain, where it has been implicated in neuronal development and survival. Mutations in the NNAT gene have been associated with neurological disorders such as epilepsy and intellectual disability. Additionally, NNAT has been identified as a potential target for the development of therapies aimed at treating neurodegenerative diseases and cancer.

GM1 gangliosidosis is a rare inherited lysosomal storage disorder caused by the deficiency of an enzyme called β-galactosidase. This enzyme is responsible for breaking down certain complex fats (gangliosides) in the body. When this enzyme is lacking or not working properly, these gangliosides accumulate in various cells, particularly in nerve cells of the brain, leading to progressive neurological deterioration.

The condition can present at different ages and with varying severity, depending on the amount of functional β-galactosidase enzyme activity. The three main types of GM1 gangliosidosis are:

1. Early infantile (type I): This is the most severe form, with symptoms appearing within the first few months of life. Infants may appear normal at birth but then develop rapidly progressing neurological problems such as developmental delay, muscle weakness, seizures, and cherry-red spots in the eyes. Life expectancy is typically less than 2 years.

2. Late infantile/juvenile (type II): Symptoms begin between ages 1 and 3 years or later in childhood. Affected individuals may have developmental delay, motor difficulties, muscle weakness, and cognitive decline. Some individuals with this form may also develop corneal clouding and bone abnormalities.

3. Adult/chronic (type III): This is the least severe form of GM1 gangliosidosis, with symptoms appearing in late childhood, adolescence, or adulthood. Symptoms can include neurological problems such as muscle weakness, tremors, and difficulties with coordination and speech.

Currently, there is no cure for GM1 gangliosidosis, and treatment is primarily supportive to manage symptoms and improve quality of life.

Mitochondrial DNA (mtDNA) is the genetic material present in the mitochondria, which are specialized structures within cells that generate energy. Unlike nuclear DNA, which is present in the cell nucleus and inherited from both parents, mtDNA is inherited solely from the mother.

MtDNA is a circular molecule that contains 37 genes, including 13 genes that encode for proteins involved in oxidative phosphorylation, a process that generates energy in the form of ATP. The remaining genes encode for rRNAs and tRNAs, which are necessary for protein synthesis within the mitochondria.

Mutations in mtDNA can lead to a variety of genetic disorders, including mitochondrial diseases, which can affect any organ system in the body. These mutations can also be used in forensic science to identify individuals and establish biological relationships.

Ubiquitination is a post-translational modification process in which a ubiquitin protein is covalently attached to a target protein. This process plays a crucial role in regulating various cellular functions, including protein degradation, DNA repair, and signal transduction. The addition of ubiquitin can lead to different outcomes depending on the number and location of ubiquitin molecules attached to the target protein. Monoubiquitination (the attachment of a single ubiquitin molecule) or multiubiquitination (the attachment of multiple ubiquitin molecules) can mark proteins for degradation by the 26S proteasome, while specific types of ubiquitination (e.g., K63-linked polyubiquitination) can serve as a signal for nonproteolytic functions such as endocytosis, autophagy, or DNA repair. Ubiquitination is a highly regulated process that involves the coordinated action of three enzymes: E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, and E3 ubiquitin ligase. Dysregulation of ubiquitination has been implicated in various diseases, including cancer, neurodegenerative disorders, and inflammatory conditions.

Glial Cell Line-Derived Neurotrophic Factor (GDNF) is a protein that plays a crucial role in the survival, development, and function of certain neurons in the nervous system. It is a member of the transforming growth factor-β (TGF-β) superfamily and was initially identified for its ability to support the survival and differentiation of midbrain dopaminergic neurons, which are critical for movement control and motivation. GDNF also supports other types of neurons, including motor neurons and sensory neurons. It exerts its effects by binding to a receptor complex consisting of GFRα1 and RET tyrosine kinase receptors, activating intracellular signaling pathways that promote neuronal survival, growth, and synaptic plasticity. GDNF has been investigated as a potential therapeutic agent for various neurodegenerative disorders, including Parkinson's disease and amyotrophic lateral sclerosis (ALS).

Proteomics is the large-scale study and analysis of proteins, including their structures, functions, interactions, modifications, and abundance, in a given cell, tissue, or organism. It involves the identification and quantification of all expressed proteins in a biological sample, as well as the characterization of post-translational modifications, protein-protein interactions, and functional pathways. Proteomics can provide valuable insights into various biological processes, diseases, and drug responses, and has applications in basic research, biomedicine, and clinical diagnostics. The field combines various techniques from molecular biology, chemistry, physics, and bioinformatics to study proteins at a systems level.

A primary cell culture is the very first cell culture generation that is established by directly isolating cells from an original tissue or organ source. These cells are removed from the body and then cultured in controlled conditions in a laboratory setting, allowing them to grow and multiply. Primary cell cultures maintain many of the characteristics of the cells in their original tissue environment, making them valuable for research purposes. However, they can only be passaged (subcultured) a limited number of times before they undergo senescence or change into a different type of cell.

The Survival Motor Neuron (SMN) complex is a protein complex that plays a crucial role in the biogenesis of small nuclear ribonucleoproteins (snRNPs), which are essential components of the spliceosome involved in pre-messenger RNA (pre-mRNA) splicing. The SMN complex consists of several proteins, including the SMN protein itself, Gemins2-8, and unrip.

The SMN protein is the central component of the complex and is encoded by the SMN1 gene located on chromosome 5q13.2. Mutations in this gene can lead to spinal muscular atrophy (SMA), a genetic disorder characterized by degeneration of motor neurons in the spinal cord, leading to muscle weakness and atrophy.

The SMN complex assembles in the cytoplasm and facilitates the assembly of spliceosomal snRNPs by helping to load Sm proteins onto small nuclear RNA (snRNA) molecules. Proper functioning of the SMN complex is essential for the correct splicing of pre-mRNA, and its dysfunction can lead to various developmental abnormalities and diseases, including SMA.

Preclinical drug evaluation refers to a series of laboratory tests and studies conducted to determine the safety and effectiveness of a new drug before it is tested in humans. These studies typically involve experiments on cells and animals to evaluate the pharmacological properties, toxicity, and potential interactions with other substances. The goal of preclinical evaluation is to establish a reasonable level of safety and understanding of how the drug works, which helps inform the design and conduct of subsequent clinical trials in humans. It's important to note that while preclinical studies provide valuable information, they may not always predict how a drug will behave in human subjects.

Central nervous system (CNS) agents are drugs or substances that act on the central nervous system, which includes the brain and spinal cord. These agents can affect the CNS in various ways, depending on their specific mechanism of action. They may be used for therapeutic purposes, such as to treat medical conditions like pain, anxiety, seizures, or sleep disorders, or they may be abused for their psychoactive effects.

CNS agents can be broadly classified into several categories based on their primary site of action and the nature of their effects. Some common categories of CNS agents include:

1. Depressants: These drugs slow down the activity of the CNS, leading to sedative, hypnotic, or anxiolytic effects. Examples include benzodiazepines, barbiturates, and sleep aids like zolpidem.
2. Stimulants: These drugs increase the activity of the CNS, leading to alertness, energy, and improved concentration. Examples include amphetamines, methylphenidate, and caffeine.
3. Analgesics: These drugs are used to treat pain and can act on various parts of the nervous system, including the peripheral nerves, spinal cord, and brain. Examples include opioids (such as morphine and oxycodone), non-opioid analgesics (such as acetaminophen and ibuprofen), and adjuvant analgesics (such as antidepressants and anticonvulsants).
4. Antiepileptics: These drugs are used to treat seizure disorders and work by modulating the electrical activity of neurons in the brain. Examples include phenytoin, carbamazepine, valproic acid, and lamotrigine.
5. Antipsychotics: These drugs are used to treat psychosis, schizophrenia, and other mental health disorders by blocking dopamine receptors in the brain. Examples include haloperidol, risperidone, and clozapine.
6. Antidepressants: These drugs are used to treat depression and anxiety disorders by modulating neurotransmitter activity in the brain. Examples include selective serotonin reuptake inhibitors (SSRIs) like fluoxetine and sertraline, tricyclic antidepressants like amitriptyline, and monoamine oxidase inhibitors (MAOIs) like phenelzine.
7. Anxiolytics: These drugs are used to treat anxiety disorders and work by modulating the activity of the neurotransmitter gamma-aminobutyric acid (GABA) in the brain. Examples include benzodiazepines like diazepam and alprazolam, and non-benzodiazepine anxiolytics like buspirone.
8. Stimulants: These drugs are used to treat attention deficit hyperactivity disorder (ADHD) and narcolepsy by increasing the activity of dopamine and norepinephrine in the brain. Examples include methylphenidate, amphetamine salts, and modafinil.
9. Sedative-hypnotics: These drugs are used to treat insomnia and other sleep disorders by depressing the activity of the central nervous system. Examples include benzodiazepines like triazolam and zolpidem, and non-benzodiazepine sedative-hypnotics like eszopiclone and ramelteon.
10. Antipsychotics: These drugs are used to treat psychotic disorders like schizophrenia, bipolar disorder, and major depressive disorder by blocking the activity of dopamine in the brain. Examples include typical antipsychotics like haloperidol and chlorpromazine, and atypical antipsychotics like risperidone and aripiprazole.
11. Antidepressants: These drugs are used to treat depression and anxiety disorders by increasing the activity of serotonin, norepinephrine, or dopamine in the brain. Examples include selective serotonin reuptake inhibitors (SSRIs) like fluoxetine and sertraline, tricyclic antidepressants like amitriptyline, and monoamine oxidase inhibitors (MAOIs) like phenelzine.
12. Anticonvulsants: These drugs are used to treat seizure disorders like epilepsy, as well as chronic pain and bipolar disorder. They work by stabilizing the electrical activity of the brain. Examples include valproic acid, lamotrigine, and carbamazepine.
13. Anxiolytics: These drugs are used to treat anxiety disorders by reducing anxiety and promoting relaxation. Examples include benzodiazepines like diazepam and alprazolam, and non-benzodiazepine anxiolytics like buspirone.
14. Hypnotics: These drugs are used to treat insomnia and other sleep disorders by promoting sleep. Examples include benzodiazepines like triazolam and temazepam, and non-benzodiazepine hypnotics like zolpidem and eszopiclone.
15. Stimulants: These drugs are used to treat attention deficit hyperactivity disorder (ADHD) and narcolepsy by increasing alertness and focus. Examples include amphetamine salts, methylphenidate, and modafinil.
16. Antihistamines: These drugs are used to treat allergies and allergic reactions by blocking the activity of histamine, a chemical that is released during an allergic response. Examples include diphenhydramine, loratadine, and cetirizine.
17. Antipsychotics: These drugs are used to treat psychosis, schizophrenia, bipolar disorder, and other mental health conditions by reducing the symptoms of these conditions. Examples include risperidone, olanzapine, and quetiapine.
18. Antidepressants: These drugs are used to treat depression, anxiety disorders, and some chronic pain conditions by increasing the levels of certain neurotransmitters in the brain. Examples include selective serotonin reuptake inhibitors (SSRIs) like fluoxetine and sertraline, and tricyclic antidepressants like amitriptyline and imipramine.
19. Anticonvulsants: These drugs are used to treat seizure disorders and some chronic pain conditions by stabilizing the electrical activity of the brain. Examples include valproic acid, lamotrigine, and carbamazepine.
20. Muscle relaxants: These drugs are used to treat muscle spasms and pain by reducing muscle tension. Examples include cyclobenzaprine, methocarbamol, and baclofen.

Genetic predisposition to disease refers to an increased susceptibility or vulnerability to develop a particular illness or condition due to inheriting specific genetic variations or mutations from one's parents. These genetic factors can make it more likely for an individual to develop a certain disease, but it does not guarantee that the person will definitely get the disease. Environmental factors, lifestyle choices, and interactions between genes also play crucial roles in determining if a genetically predisposed person will actually develop the disease. It is essential to understand that having a genetic predisposition only implies a higher risk, not an inevitable outcome.

Exons are the coding regions of DNA that remain in the mature, processed mRNA after the removal of non-coding intronic sequences during RNA splicing. These exons contain the information necessary to encode proteins, as they specify the sequence of amino acids within a polypeptide chain. The arrangement and order of exons can vary between different genes and even between different versions of the same gene (alternative splicing), allowing for the generation of multiple protein isoforms from a single gene. This complexity in exon structure and usage significantly contributes to the diversity and functionality of the proteome.

Endoplasmic reticulum (ER) stress refers to a cellular condition characterized by the accumulation of misfolded or unfolded proteins within the ER lumen, leading to disruption of its normal functions. The ER is a membrane-bound organelle responsible for protein folding, modification, and transport, as well as lipid synthesis and calcium homeostasis. Various physiological and pathological conditions can cause an imbalance between the rate of protein entry into the ER and its folding capacity, resulting in ER stress.

To cope with this stress, cells have evolved a set of signaling pathways called the unfolded protein response (UPR). The UPR aims to restore ER homeostasis by reducing global protein synthesis, enhancing ER-associated degradation (ERAD) of misfolded proteins, and upregulating the expression of genes involved in protein folding, modification, and quality control.

The UPR is mediated by three major signaling branches:

1. Inositol-requiring enzyme 1α (IRE1α): IRE1α is an ER transmembrane protein with endoribonuclease activity that catalyzes the splicing of X-box binding protein 1 (XBP1) mRNA, leading to the expression of a potent transcription factor, spliced XBP1 (sXBP1). sXBP1 upregulates genes involved in ERAD and protein folding.
2. Activating transcription factor 6 (ATF6): ATF6 is an ER transmembrane protein that, upon ER stress, undergoes proteolytic cleavage to release its cytoplasmic domain, which acts as a potent transcription factor. ATF6 upregulates genes involved in protein folding and degradation.
3. Protein kinase R-like endoplasmic reticulum kinase (PERK): PERK is an ER transmembrane protein that phosphorylates the α subunit of eukaryotic initiation factor 2 (eIF2α) upon ER stress, leading to a global reduction in protein synthesis and preferential translation of activating transcription factor 4 (ATF4). ATF4 upregulates genes involved in amino acid metabolism, redox homeostasis, and apoptosis.

These three branches of the UPR work together to restore ER homeostasis by increasing protein folding capacity, reducing global protein synthesis, and promoting degradation of misfolded proteins. However, if the stress persists or becomes too severe, the UPR can trigger cell death through apoptosis.

In summary, the unfolded protein response (UPR) is a complex signaling network that helps maintain ER homeostasis by detecting and responding to the accumulation of misfolded proteins in the ER lumen. The UPR involves three main branches: IRE1α, ATF6, and PERK, which work together to restore ER homeostasis through increased protein folding capacity, reduced global protein synthesis, and enhanced degradation of misfolded proteins. Persistent or severe ER stress can lead to the activation of cell death pathways by the UPR.

Iron metabolism disorders are a group of medical conditions that affect the body's ability to absorb, transport, store, or utilize iron properly. Iron is an essential nutrient that plays a crucial role in various bodily functions, including oxygen transportation and energy production. However, imbalances in iron levels can lead to several health issues.

There are two main types of iron metabolism disorders:

1. Iron deficiency anemia (IDA): This condition occurs when the body lacks adequate iron to produce sufficient amounts of hemoglobin, a protein in red blood cells responsible for carrying oxygen throughout the body. Causes of IDA may include inadequate dietary iron intake, blood loss, or impaired iron absorption due to conditions like celiac disease or inflammatory bowel disease.
2. Hemochromatosis: This is a genetic disorder characterized by excessive absorption and accumulation of iron in various organs, including the liver, heart, and pancreas. Over time, this excess iron can lead to organ damage and diseases such as cirrhosis, heart failure, diabetes, and arthritis. Hemochromatosis is typically caused by mutations in the HFE gene, which regulates iron absorption in the intestines.

Other iron metabolism disorders include:

* Anemia of chronic disease (ACD): A type of anemia that occurs in individuals with chronic inflammation or infection, where iron is not efficiently used for hemoglobin production due to altered regulation.
* Sideroblastic anemias: These are rare disorders characterized by the abnormal formation of ringed sideroblasts (immature red blood cells containing iron-laden mitochondria) in the bone marrow, leading to anemia and other symptoms.
* Iron-refractory iron deficiency anemia (IRIDA): A rare inherited disorder caused by mutations in the TMPRSS6 gene, resulting in impaired regulation of hepcidin, a hormone that controls iron absorption and distribution in the body. This leads to both iron deficiency and iron overload.

Proper diagnosis and management of iron metabolism disorders are essential to prevent complications and maintain overall health. Treatment options may include dietary modifications, iron supplementation, phlebotomy (bloodletting), or chelation therapy, depending on the specific disorder and its severity.

"Postmortem changes," also known as "autolysis" or "decomposition," refer to the natural biological processes that occur in a deceased body after death. These changes include various chemical, physical, and biological alterations such as livor mortis (pooling of blood), algor mortis (drop in body temperature), rigor mortis (stiffening of muscles), putrefaction (breakdown by microorganisms), and decomposition by insects and other animals. These changes help forensic experts estimate the time since death, known as the postmortem interval.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Kymography is a medical imaging technique used to visualize and analyze the movement or motion of structures, such as muscles, blood vessels, or intestines, over time. It involves capturing a series of images at high temporal resolution and then displaying them in a way that emphasizes changes in intensity along a single line or region of interest.

In kymography, a moving stripe or band is created on the image display, representing the movement of the structure being studied. The resulting image shows the velocity, direction, and patterns of motion of the structure, which can be useful for diagnostic purposes or for research in physiology and biomechanics.

Kymography is often used in conjunction with other imaging techniques, such as ultrasound or fluoroscopy, to provide more detailed information about the function and behavior of different tissues and organs.

The Unfolded Protein Response (UPR) is a cellular stress response pathway that is activated when the endoplasmic reticulum (ER), an organelle responsible for protein folding and processing, becomes overwhelmed with misfolded or unfolded proteins. The UPR is initiated by three ER transmembrane sensors: IRE1, PERK, and ATF6. These sensors detect the accumulation of unfolded proteins in the ER lumen and transmit signals to the nucleus to induce a variety of adaptive responses aimed at restoring ER homeostasis.

These responses include:

* Transcriptional upregulation of genes encoding chaperones, folding enzymes, and components of the ER-associated degradation (ERAD) machinery to enhance protein folding capacity and promote the clearance of misfolded proteins.
* Attenuation of global protein synthesis to reduce the influx of new proteins into the ER.
* Activation of autophagy, a process that helps eliminate damaged organelles and aggregated proteins.

If these adaptive responses are insufficient to restore ER homeostasis, the UPR can also trigger apoptosis, or programmed cell death, as a last resort to eliminate damaged cells and prevent the spread of protein misfolding diseases such as neurodegenerative disorders.

The cell nucleus is a membrane-bound organelle found in the eukaryotic cells (cells with a true nucleus). It contains most of the cell's genetic material, organized as DNA molecules in complex with proteins, RNA molecules, and histones to form chromosomes.

The primary function of the cell nucleus is to regulate and control the activities of the cell, including growth, metabolism, protein synthesis, and reproduction. It also plays a crucial role in the process of mitosis (cell division) by separating and protecting the genetic material during this process. The nuclear membrane, or nuclear envelope, surrounding the nucleus is composed of two lipid bilayers with numerous pores that allow for the selective transport of molecules between the nucleoplasm (nucleus interior) and the cytoplasm (cell exterior).

The cell nucleus is a vital structure in eukaryotic cells, and its dysfunction can lead to various diseases, including cancer and genetic disorders.

Clioquinol is an antimicrobial drug that contains a combination of clioquinal and hydrocortisone acetate. It is used topically to treat various skin infections and inflammatory conditions. Clioquinol has antibacterial and antifungal properties, while hydrocortisone acetate is a corticosteroid that reduces inflammation and suppresses the immune response.

Clioquinol was first synthesized in the 1930s and was widely used as an antidiarrheal medication until it was banned in many countries due to its association with a neurological disorder called subacute myelooptic neuropathy (SMON). However, topical clioquinol is still available in some countries for the treatment of skin conditions.

It's important to note that topical clioquinol should be used with caution and under the supervision of a healthcare professional, as it can cause skin irritation and sensitization in some individuals. Additionally, prolonged or excessive use of corticosteroids like hydrocortisone acetate can lead to thinning of the skin, increased susceptibility to infection, and other adverse effects.

Alpha-Crystallin B chain is a protein that is a component of the eye lens. It is one of the two subunits of the alpha-crystallin protein, which is a major structural protein in the lens and helps to maintain the transparency and refractive properties of the lens. Alpha-Crystallin B chain is produced by the CRYAB gene and has chaperone-like properties, helping to prevent the aggregation of other proteins and contributing to the maintenance of lens clarity. Mutations in the CRYAB gene can lead to various eye disorders, including cataracts and certain types of glaucoma.

Physiological stress is a response of the body to a demand or threat that disrupts homeostasis and activates the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis. This results in the release of stress hormones such as adrenaline, cortisol, and noradrenaline, which prepare the body for a "fight or flight" response. Increased heart rate, rapid breathing, heightened sensory perception, and increased alertness are some of the physiological changes that occur during this response. Chronic stress can have negative effects on various bodily functions, including the immune, cardiovascular, and nervous systems.

DEAD-Box Protein 20 (DDX20) is a member of the DEAD-box protein family, which are named for the conserved amino acid sequence "Asp-Glu-Ala-Asp" within their helicase domains. These proteins are involved in various aspects of RNA metabolism, including splicing, transport, translation, and degradation.

DDX20, also known as p68 or DP103, is a DNA/RNA helicase that plays a role in transcriptional regulation, pre-mRNA processing, and RNA export. It has been implicated in several cellular processes, including cell cycle progression, differentiation, and apoptosis. DDX20 can interact with various proteins involved in transcription, such as RNA polymerase II and the basal transcription factor TFIID, as well as components of the spliceosome and other RNA-binding proteins.

Mutations or dysregulation of DDX20 have been associated with several human diseases, including cancer, neurodevelopmental disorders, and autoimmune diseases. For example, increased expression of DDX20 has been observed in various types of cancer, such as breast, lung, and ovarian cancers, and may contribute to tumor progression by promoting cell proliferation and inhibiting apoptosis. Additionally, mutations in the gene encoding DDX20 have been identified in patients with intellectual disability, epilepsy, and autism spectrum disorder.

Axotomy is a medical term that refers to the surgical cutting or severing of an axon, which is the long, slender projection of a neuron (nerve cell) that conducts electrical impulses away from the cell body and toward other cells. Axons are a critical component of the nervous system, allowing for communication between different parts of the body.

Axotomy is often used in research settings to study the effects of axonal injury on neuronal function and regeneration. This procedure can provide valuable insights into the mechanisms underlying neurodegenerative disorders and potential therapies for nerve injuries. However, it is important to note that axotomy can also have significant consequences for the affected neuron, including changes in gene expression, metabolism, and overall survival.

A tremor is an involuntary, rhythmic muscle contraction and relaxation that causes a shaking movement. It's a type of motion disorder that can affect any part of your body, but it most often occurs in your hands. Tremors can be harmless, but they can also be a symptom of a more serious neurological disorder. The cause of tremors isn't always known, but they can be the result of damage to the brain from a stroke, multiple sclerosis, or trauma. Certain medications, alcohol abuse, and drug withdrawal can also cause tremors. In some cases, tremors may be inherited and run in families.

Tremors can be classified based on their cause, appearance, and the situation in which they occur. The two most common types of tremors are:

* Resting tremors, which occur when your muscles are relaxed, such as when your hands are resting on your lap. Parkinson's disease is a common cause of this type of tremor.
* Action tremors, which occur with purposeful movement, such as when you're trying to hold something or when you're using a utensil. Essential tremor, the most common type of tremor, is an action tremor.

Tremors can also be classified based on their frequency (how often they occur) and amplitude (the size of the movement). High-frequency tremors are faster and smaller in amplitude, while low-frequency tremors are slower and larger in amplitude.

In general, tremors are not a life-threatening condition, but they can be embarrassing or make it difficult to perform daily activities. In some cases, tremors may indicate a more serious underlying condition that requires treatment. If you're concerned about tremors or have any questions about your symptoms, it's important to speak with a healthcare provider for an accurate diagnosis and appropriate treatment.

"Cell count" is a medical term that refers to the process of determining the number of cells present in a given volume or sample of fluid or tissue. This can be done through various laboratory methods, such as counting individual cells under a microscope using a specialized grid called a hemocytometer, or using automated cell counters that use light scattering and electrical impedance techniques to count and classify different types of cells.

Cell counts are used in a variety of medical contexts, including hematology (the study of blood and blood-forming tissues), microbiology (the study of microscopic organisms), and pathology (the study of diseases and their causes). For example, a complete blood count (CBC) is a routine laboratory test that includes a white blood cell (WBC) count, red blood cell (RBC) count, hemoglobin level, hematocrit value, and platelet count. Abnormal cell counts can indicate the presence of various medical conditions, such as infections, anemia, or leukemia.

Survival of Motor Neuron 2 (SMN2) protein is a functional copy of the Survival of Motor Neuron (SMN) protein, which is produced from the SMN2 gene. The SMN protein is crucial for the survival of motor neurons, the nerve cells that control muscle movement. In people with spinal muscular atrophy (SMA), a genetic disorder that causes progressive muscle weakness and loss of movement, there is a mutation in the main SMN1 gene that leads to reduced levels of functional SMN protein.

The SMN2 gene can also produce some functional SMN protein, but it mainly produces an unstable, truncated form of the protein due to a critical difference in its exon 7 splicing pattern. However, a small percentage (about 10-15%) of SMN2 transcripts can be correctly spliced and produce full-length, functional SMN protein. The amount of functional SMN protein produced from the SMN2 gene is directly related to the severity of SMA; more SMN protein production from SMN2 leads to less severe symptoms. Therefore, therapies aimed at increasing SMN2-derived SMN protein levels are being developed and tested for the treatment of SMA.

An amino acid substitution is a type of mutation in which one amino acid in a protein is replaced by another. This occurs when there is a change in the DNA sequence that codes for a particular amino acid in a protein. The genetic code is redundant, meaning that most amino acids are encoded by more than one codon (a sequence of three nucleotides). As a result, a single base pair change in the DNA sequence may not necessarily lead to an amino acid substitution. However, if a change does occur, it can have a variety of effects on the protein's structure and function, depending on the nature of the substituted amino acids. Some substitutions may be harmless, while others may alter the protein's activity or stability, leading to disease.

Cerebellar ataxia is a type of ataxia, which refers to a group of disorders that cause difficulties with coordination and movement. Cerebellar ataxia specifically involves the cerebellum, which is the part of the brain responsible for maintaining balance, coordinating muscle movements, and regulating speech and eye movements.

The symptoms of cerebellar ataxia may include:

* Unsteady gait or difficulty walking
* Poor coordination of limb movements
* Tremors or shakiness, especially in the hands
* Slurred or irregular speech
* Abnormal eye movements, such as nystagmus (rapid, involuntary movement of the eyes)
* Difficulty with fine motor tasks, such as writing or buttoning a shirt

Cerebellar ataxia can be caused by a variety of underlying conditions, including:

* Genetic disorders, such as spinocerebellar ataxia or Friedreich's ataxia
* Brain injury or trauma
* Stroke or brain hemorrhage
* Infections, such as meningitis or encephalitis
* Exposure to toxins, such as alcohol or certain medications
* Tumors or other growths in the brain

Treatment for cerebellar ataxia depends on the underlying cause. In some cases, there may be no cure, and treatment is focused on managing symptoms and improving quality of life. Physical therapy, occupational therapy, and speech therapy can help improve coordination, balance, and communication skills. Medications may also be used to treat specific symptoms, such as tremors or muscle spasticity. In some cases, surgery may be recommended to remove tumors or repair damage to the brain.

Movement disorders are a group of neurological conditions that affect the control and coordination of voluntary movements. These disorders can result from damage to or dysfunction of the cerebellum, basal ganglia, or other parts of the brain that regulate movement. Symptoms may include tremors, rigidity, bradykinesia (slowness of movement), akathisia (restlessness and inability to remain still), dystonia (sustained muscle contractions leading to abnormal postures), chorea (rapid, unpredictable movements), tics, and gait disturbances. Examples of movement disorders include Parkinson's disease, Huntington's disease, Tourette syndrome, and dystonic disorders.

Lipid peroxidation is a process in which free radicals, such as reactive oxygen species (ROS), steal electrons from lipids containing carbon-carbon double bonds, particularly polyunsaturated fatty acids (PUFAs). This results in the formation of lipid hydroperoxides, which can decompose to form a variety of compounds including reactive carbonyl compounds, aldehydes, and ketones.

Malondialdehyde (MDA) is one such compound that is commonly used as a marker for lipid peroxidation. Lipid peroxidation can cause damage to cell membranes, leading to changes in their fluidity and permeability, and can also result in the modification of proteins and DNA, contributing to cellular dysfunction and ultimately cell death. It is associated with various pathological conditions such as atherosclerosis, neurodegenerative diseases, and cancer.

Excitatory Amino Acid Transporter 2 (EAAT2) is a type of glutamate transporter protein found in the membranes of glial cells in the central nervous system. Glutamate is the primary excitatory neurotransmitter in the brain, and its levels must be carefully regulated to maintain normal neuronal function and survival. EAAT2 plays a critical role in this regulation by removing excess glutamate from the synaptic cleft and returning it to glial cells for storage or breakdown.

EAAT2 is responsible for the majority of glutamate reuptake in the brain, and its expression and function are crucial for maintaining proper neuronal excitability and preventing excitotoxicity, a form of neurodegeneration that can occur when glutamate levels become too high. Mutations or dysfunction in EAAT2 have been implicated in several neurological disorders, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and epilepsy.

Paraparesis, spastic type, is a medical term used to describe a condition characterized by partial weakness or loss of voluntary movement in the lower extremities (legs). The term "paraparesis" comes from Greek words "para" meaning beside or beyond, and "paresis" meaning loosening or relaxation.

In spastic paraparesis, the muscle tone is increased, causing stiffness and resistance to movement, particularly during quick or forceful movements. This increased muscle tone, also known as spasticity, results from an upper motor neuron lesion in the brain or spinal cord that affects the corticospinal tract, which carries signals from the brain to the muscles.

Spastic paraparesis can be caused by various conditions, including spinal cord injuries, multiple sclerosis, hereditary spastic paraplegia, and stroke, among others. The severity of symptoms may vary widely, ranging from mild weakness to complete paralysis. Treatment options for spastic paraparesis depend on the underlying cause and may include physical therapy, medications, surgery, or a combination of these approaches.

Histone deacetylases (HDACs) are a group of enzymes that play a crucial role in the regulation of gene expression. They work by removing acetyl groups from histone proteins, which are the structural components around which DNA is wound to form chromatin, the material that makes up chromosomes.

Histone acetylation is a modification that generally results in an "open" chromatin structure, allowing for the transcription of genes into proteins. When HDACs remove these acetyl groups, the chromatin becomes more compact and gene expression is reduced or silenced.

HDACs are involved in various cellular processes, including development, differentiation, and survival. Dysregulation of HDAC activity has been implicated in several diseases, such as cancer, neurodegenerative disorders, and cardiovascular diseases. As a result, HDAC inhibitors have emerged as promising therapeutic agents for these conditions.

RNA interference (RNAi) is a biological process in which RNA molecules inhibit the expression of specific genes. This process is mediated by small RNA molecules, including microRNAs (miRNAs) and small interfering RNAs (siRNAs), that bind to complementary sequences on messenger RNA (mRNA) molecules, leading to their degradation or translation inhibition.

RNAi plays a crucial role in regulating gene expression and defending against foreign genetic elements, such as viruses and transposons. It has also emerged as an important tool for studying gene function and developing therapeutic strategies for various diseases, including cancer and viral infections.

Carrier proteins, also known as transport proteins, are a type of protein that facilitates the movement of molecules across cell membranes. They are responsible for the selective and active transport of ions, sugars, amino acids, and other molecules from one side of the membrane to the other, against their concentration gradient. This process requires energy, usually in the form of ATP (adenosine triphosphate).

Carrier proteins have a specific binding site for the molecule they transport, and undergo conformational changes upon binding, which allows them to move the molecule across the membrane. Once the molecule has been transported, the carrier protein returns to its original conformation, ready to bind and transport another molecule.

Carrier proteins play a crucial role in maintaining the balance of ions and other molecules inside and outside of cells, and are essential for many physiological processes, including nerve impulse transmission, muscle contraction, and nutrient uptake.

Canavan disease is a rare, inherited genetic disorder that affects the white matter (the nerve cells that transmit nerve impulses) in the brain. It is caused by mutations in the gene for an enzyme called aspartoacylase, which is responsible for breaking down a compound called N-acetylaspartic acid (NAA) in the brain. As a result of this genetic defect, NAA accumulates to toxic levels in the brain, leading to progressive damage to the white matter and resulting in a number of neurological symptoms.

Canavan disease is typically diagnosed in infancy or early childhood, and it affects both boys and girls. The symptoms of Canavan disease can vary widely, but they often include developmental delays, hypotonia (low muscle tone), difficulty with movements and balance, seizures, and optic atrophy (degeneration of the optic nerve). As the disease progresses, individuals with Canavan disease may lose previously acquired skills, such as the ability to sit, stand, or walk.

There is currently no cure for Canavan disease, and treatment is focused on managing the symptoms and supporting the individual's overall health and well-being. Physical therapy, occupational therapy, and speech therapy can help improve motor function and communication skills, while medications may be used to control seizures and other symptoms. In some cases, individuals with Canavan disease may require assistive devices, such as wheelchairs or communication aids, to help them navigate their environment and communicate with others.

Recombinant proteins are artificially created proteins produced through the use of recombinant DNA technology. This process involves combining DNA molecules from different sources to create a new set of genes that encode for a specific protein. The resulting recombinant protein can then be expressed, purified, and used for various applications in research, medicine, and industry.

Recombinant proteins are widely used in biomedical research to study protein function, structure, and interactions. They are also used in the development of diagnostic tests, vaccines, and therapeutic drugs. For example, recombinant insulin is a common treatment for diabetes, while recombinant human growth hormone is used to treat growth disorders.

The production of recombinant proteins typically involves the use of host cells, such as bacteria, yeast, or mammalian cells, which are engineered to express the desired protein. The host cells are transformed with a plasmid vector containing the gene of interest, along with regulatory elements that control its expression. Once the host cells are cultured and the protein is expressed, it can be purified using various chromatography techniques.

Overall, recombinant proteins have revolutionized many areas of biology and medicine, enabling researchers to study and manipulate proteins in ways that were previously impossible.

A mammalian embryo is the developing offspring of a mammal, from the time of implantation of the fertilized egg (blastocyst) in the uterus until the end of the eighth week of gestation. During this period, the embryo undergoes rapid cell division and organ differentiation to form a complex structure with all the major organs and systems in place. This stage is followed by fetal development, which continues until birth. The study of mammalian embryos is important for understanding human development, evolution, and reproductive biology.

Sirtuins are a family of proteins that possess NAD+-dependent deacetylase or ADP-ribosyltransferase activity. They play crucial roles in regulating various cellular processes, such as aging, transcription, apoptosis, inflammation, and stress resistance. In humans, there are seven known sirtuins (SIRT1-7), each with distinct subcellular localizations and functions. SIRT1, the most well-studied sirtuin, is a nuclear protein involved in chromatin remodeling, DNA repair, and metabolic regulation. Other sirtuins are found in various cellular compartments, including the nucleus, cytoplasm, and mitochondria, where they modulate specific targets to maintain cellular homeostasis. Dysregulation of sirtuins has been implicated in several diseases, including cancer, diabetes, and neurodegenerative disorders.

Excitatory amino acid agonists are substances that bind to and activate excitatory amino acid receptors, leading to an increase in the excitation or activation of neurons. The most common excitatory amino acids in the central nervous system are glutamate and aspartate.

Agonists of excitatory amino acid receptors can be divided into two main categories: ionotropic and metabotropic. Ionotropic receptors, such as N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors, are ligand-gated ion channels that directly mediate fast excitatory synaptic transmission. Metabotropic receptors, on the other hand, are G protein-coupled receptors that modulate synaptic activity through second messenger systems.

Excitatory amino acid agonists have been implicated in various physiological and pathophysiological processes, including learning and memory, neurodevelopment, and neurodegenerative disorders such as stroke, epilepsy, and Alzheimer's disease. They are also used in research to study the functions of excitatory amino acid receptors and their roles in neuronal signaling. However, due to their potential neurotoxic effects, the therapeutic use of excitatory amino acid agonists is limited.

Mitochondrial membrane potential is the electric potential difference (voltage) across the inner mitochondrial membrane. It is negative inside the mitochondria and positive outside. This electrical gradient is established by the active transport of hydrogen ions (protons) out of the mitochondrial matrix and into the intermembrane space by complexes in the electron transport chain during oxidative phosphorylation. The energy stored in this electrochemical gradient is used to generate ATP, which is the main source of energy for cellular metabolism.

Glutathione is a tripeptide composed of three amino acids: cysteine, glutamic acid, and glycine. It is a vital antioxidant that plays an essential role in maintaining cellular health and function. Glutathione helps protect cells from oxidative stress by neutralizing free radicals, which are unstable molecules that can damage cells and contribute to aging and diseases such as cancer, heart disease, and dementia. It also supports the immune system, detoxifies harmful substances, and regulates various cellular processes, including DNA synthesis and repair.

Glutathione is found in every cell of the body, with particularly high concentrations in the liver, lungs, and eyes. The body can produce its own glutathione, but levels may decline with age, illness, or exposure to toxins. As such, maintaining optimal glutathione levels through diet, supplementation, or other means is essential for overall health and well-being.

Immunoprecipitation (IP) is a research technique used in molecular biology and immunology to isolate specific antigens or antibodies from a mixture. It involves the use of an antibody that recognizes and binds to a specific antigen, which is then precipitated out of solution using various methods, such as centrifugation or chemical cross-linking.

In this technique, an antibody is first incubated with a sample containing the antigen of interest. The antibody specifically binds to the antigen, forming an immune complex. This complex can then be captured by adding protein A or G agarose beads, which bind to the constant region of the antibody. The beads are then washed to remove any unbound proteins, leaving behind the precipitated antigen-antibody complex.

Immunoprecipitation is a powerful tool for studying protein-protein interactions, post-translational modifications, and signal transduction pathways. It can also be used to detect and quantify specific proteins in biological samples, such as cells or tissues, and to identify potential biomarkers of disease.

Niemann-Pick diseases are a group of inherited metabolic disorders characterized by the accumulation of lipids, particularly sphingomyelin and cholesterol, within cells due to deficiencies in certain enzymes. These diseases are caused by mutations in the SMPD1, NPC1, or NPC2 genes, among others. There are four main types of Niemann-Pick disease (Types A, B, C, and D), each with varying severity and symptoms.

Type A and Type B diseases, also known as Acid Sphingomyelinase Deficiency or ASMD, result from mutations in the SMPD1 gene leading to a deficiency of acid sphingomyelinase enzyme. This causes excessive accumulation of sphingomyelin in various tissues, particularly in the liver, spleen, lungs, and brain.

Type A is the most severe form, typically presenting in infancy with symptoms such as developmental delay, feeding difficulties, enlarged liver and spleen, lung infection, and progressive neurological degeneration, which often leads to early death, usually before age 3.

Type B has a broader range of severity and onset, from infancy to adulthood. Symptoms may include enlarged liver and spleen, lung disease, poor growth, and varying degrees of neurological impairment. Type B patients can survive into adolescence or adulthood, depending on the severity of their symptoms.

Type C and Type D diseases, also known as Niemann-Pick Type C Disease (NPC), are caused by mutations in either the NPC1 or NPC2 genes, leading to defective intracellular lipid transport. This results in excessive accumulation of cholesterol and other lipids within cells, particularly in the brain, liver, spleen, and lungs.

Type C typically presents in childhood but can also manifest in adolescence or adulthood. Symptoms include progressive neurological degeneration, ataxia, seizures, dementia, problems with speech and swallowing, and yellowish skin (jaundice) at birth or during infancy due to liver involvement. Type C patients usually have a shorter life expectancy, often surviving into their teens, twenties, or thirties.

Type D is a subtype of NPC that affects people of Nova Scotian descent and has similar symptoms to Type C but with an earlier onset and faster progression.

Genetic therapy, also known as gene therapy, is a medical intervention that involves the use of genetic material, such as DNA or RNA, to treat or prevent diseases. It works by introducing functional genes into cells to replace missing or faulty ones caused by genetic disorders or mutations. The introduced gene is incorporated into the recipient's genome, allowing for the production of a therapeutic protein that can help manage the disease symptoms or even cure the condition.

There are several approaches to genetic therapy, including:

1. Replacing a faulty gene with a healthy one
2. Inactivating or "silencing" a dysfunctional gene causing a disease
3. Introducing a new gene into the body to help fight off a disease, such as cancer

Genetic therapy holds great promise for treating various genetic disorders, including cystic fibrosis, muscular dystrophy, hemophilia, and certain types of cancer. However, it is still an evolving field with many challenges, such as efficient gene delivery, potential immune responses, and ensuring the safety and long-term effectiveness of the therapy.

Calpains are a family of calcium-dependent cysteine proteases that play important roles in various cellular processes, including signal transduction, cell death, and remodeling of the cytoskeleton. They are present in most tissues and can be activated by an increase in intracellular calcium levels. There are at least 15 different calpain isoforms identified in humans, which are categorized into two groups based on their calcium requirements for activation: classical calpains (calpain-1 and calpain-2) and non-classical calpains (calpain-3 to calpain-15). Dysregulation of calpain activity has been implicated in several pathological conditions, such as neurodegenerative diseases, muscular dystrophies, and cancer.

HeLa cells are a type of immortalized cell line used in scientific research. They are derived from a cancer that developed in the cervical tissue of Henrietta Lacks, an African-American woman, in 1951. After her death, cells taken from her tumor were found to be capable of continuous division and growth in a laboratory setting, making them an invaluable resource for medical research.

HeLa cells have been used in a wide range of scientific studies, including research on cancer, viruses, genetics, and drug development. They were the first human cell line to be successfully cloned and are able to grow rapidly in culture, doubling their population every 20-24 hours. This has made them an essential tool for many areas of biomedical research.

It is important to note that while HeLa cells have been instrumental in numerous scientific breakthroughs, the story of their origin raises ethical questions about informed consent and the use of human tissue in research.

AIDS Dementia Complex (ADC) is a neurological disorder that occurs in people with advanced HIV infection or AIDS. It is also known as HIV-associated dementia (HAD) or HIV encephalopathy. ADC is characterized by cognitive impairment, motor dysfunction, and behavioral changes that can significantly affect the individual's daily functioning and quality of life.

The symptoms of AIDS Dementia Complex may include:
- Difficulty with concentration and memory
- Slowness in thinking, processing information, or making decisions
- Changes in mood or personality, such as depression, irritability, or apathy
- Difficulty with coordination, balance, or speech
- Progressive weakness and wasting of muscles
- Difficulty with swallowing or speaking

The exact cause of ADC is not fully understood, but it is believed to be related to the direct effects of HIV on the brain. The virus can infect and damage nerve cells, leading to inflammation and degeneration of brain tissue. Treatment for ADC typically involves antiretroviral therapy (ART) to control HIV replication, as well as medications to manage specific symptoms. In some cases, supportive care such as physical therapy or occupational therapy may also be recommended.

Atrophic muscular disorders are medical conditions that involve the progressive loss of muscle mass and weakness due to the degeneration of muscle tissue. This process occurs because of a decrease in the size or number of muscle fibers, which can be caused by various factors such as nerve damage, lack of use, or underlying diseases.

There are two main types of atrophic muscular disorders: neurogenic and myopathic. Neurogenic atrophy is caused by damage to the nerves that supply the muscles, leading to muscle weakness and wasting. Examples of conditions that can cause neurogenic atrophy include motor neuron disease, spinal cord injury, and peripheral neuropathy.

Myopathic atrophy, on the other hand, is caused by primary muscle diseases that affect the muscle fibers themselves. Conditions such as muscular dystrophy, metabolic myopathies, and inflammatory myopathies can all lead to myopathic atrophy.

Symptoms of atrophic muscular disorders may include muscle weakness, wasting, cramping, spasms, and difficulty with movement and coordination. Treatment for these conditions depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, the damage to the muscles may be irreversible, and the goal of treatment is to manage symptoms and maintain function as much as possible.

Apoferritins are the protein shells or apoproteins of ferritin molecules that are devoid of iron. Ferritin is a protein in cells that stores iron and releases it in a form that can be used by the body. Apoferritin can bind with iron ions to form ferritin. It has a hollow, spherical structure and is often used as a model for studying protein folding and assembly.

Nerve regeneration is the process of regrowth and restoration of functional nerve connections following damage or injury to the nervous system. This complex process involves various cellular and molecular events, such as the activation of support cells called glia, the sprouting of surviving nerve fibers (axons), and the reformation of neural circuits. The goal of nerve regeneration is to enable the restoration of normal sensory, motor, and autonomic functions impaired due to nerve damage or injury.

In situ nick-end labeling (ISEL, also known as TUNEL) is a technique used in pathology and molecular biology to detect DNA fragmentation, which is a characteristic of apoptotic cells (cells undergoing programmed cell death). The method involves labeling the 3'-hydroxyl termini of double or single stranded DNA breaks in situ (within tissue sections or individual cells) using modified nucleotides that are coupled to a detectable marker, such as a fluorophore or an enzyme. This technique allows for the direct visualization and quantification of apoptotic cells within complex tissues or cell populations.

Microtubules are hollow, cylindrical structures composed of tubulin proteins in the cytoskeleton of eukaryotic cells. They play crucial roles in various cellular processes such as maintaining cell shape, intracellular transport, and cell division (mitosis and meiosis). Microtubules are dynamic, undergoing continuous assembly and disassembly, which allows them to rapidly reorganize in response to cellular needs. They also form part of important cellular structures like centrioles, basal bodies, and cilia/flagella.

A disease is a condition that impairs normal functioning and causes harm to the body. It is typically characterized by a specific set of symptoms and may be caused by genetic, environmental, or infectious agents. A disease can also be described as a disorder of structure or function in an organism that produces specific signs or symptoms. Diseases can range from minor ones, like the common cold, to serious illnesses, such as heart disease or cancer. They can also be acute, with a sudden onset and short duration, or chronic, lasting for a long period of time. Ultimately, a disease is any deviation from normal homeostasis that causes harm to an organism.

Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.

A case-control study is an observational research design used to identify risk factors or causes of a disease or health outcome. In this type of study, individuals with the disease or condition (cases) are compared with similar individuals who do not have the disease or condition (controls). The exposure history or other characteristics of interest are then compared between the two groups to determine if there is an association between the exposure and the disease.

Case-control studies are often used when it is not feasible or ethical to conduct a randomized controlled trial, as they can provide valuable insights into potential causes of diseases or health outcomes in a relatively short period of time and at a lower cost than other study designs. However, because case-control studies rely on retrospective data collection, they are subject to biases such as recall bias and selection bias, which can affect the validity of the results. Therefore, it is important to carefully design and conduct case-control studies to minimize these potential sources of bias.

Cognition refers to the mental processes involved in acquiring, processing, and utilizing information. These processes include perception, attention, memory, language, problem-solving, and decision-making. Cognitive functions allow us to interact with our environment, understand and respond to stimuli, learn new skills, and remember experiences.

In a medical context, cognitive function is often assessed as part of a neurological or psychiatric evaluation. Impairments in cognition can be caused by various factors, such as brain injury, neurodegenerative diseases (e.g., Alzheimer's disease), infections, toxins, and mental health conditions. Assessing cognitive function helps healthcare professionals diagnose conditions, monitor disease progression, and develop treatment plans.

"Drug design" is the process of creating and developing a new medication or therapeutic agent to treat or prevent a specific disease or condition. It involves identifying potential targets within the body, such as proteins or enzymes that are involved in the disease process, and then designing small molecules or biologics that can interact with these targets to produce a desired effect.

The drug design process typically involves several stages, including:

1. Target identification: Researchers identify a specific molecular target that is involved in the disease process.
2. Lead identification: Using computational methods and high-throughput screening techniques, researchers identify small molecules or biologics that can interact with the target.
3. Lead optimization: Researchers modify the chemical structure of the lead compound to improve its ability to interact with the target, as well as its safety and pharmacokinetic properties.
4. Preclinical testing: The optimized lead compound is tested in vitro (in a test tube or petri dish) and in vivo (in animals) to evaluate its safety and efficacy.
5. Clinical trials: If the preclinical testing is successful, the drug moves on to clinical trials in humans to further evaluate its safety and efficacy.

The ultimate goal of drug design is to create a new medication that is safe, effective, and can be used to improve the lives of patients with a specific disease or condition.

Drug discovery is the process of identifying new chemical entities or biological agents that have the potential to be used as therapeutic or preventive treatments for diseases. This process involves several stages, including target identification, lead identification, hit-to-lead optimization, lead optimization, preclinical development, and clinical trials.

Target identification is the initial stage of drug discovery, where researchers identify a specific molecular target, such as a protein or gene, that plays a key role in the disease process. Lead identification involves screening large libraries of chemical compounds or natural products to find those that interact with the target molecule and have potential therapeutic activity.

Hit-to-lead optimization is the stage where researchers optimize the chemical structure of the lead compound to improve its potency, selectivity, and safety profile. Lead optimization involves further refinement of the compound's structure to create a preclinical development candidate. Preclinical development includes studies in vitro (in test tubes or petri dishes) and in vivo (in animals) to evaluate the safety, efficacy, and pharmacokinetics of the drug candidate.

Clinical trials are conducted in human volunteers to assess the safety, tolerability, and efficacy of the drug candidate in treating the disease. If the drug is found to be safe and effective in clinical trials, it may be approved by regulatory agencies such as the U.S. Food and Drug Administration (FDA) for use in patients.

Overall, drug discovery is a complex and time-consuming process that requires significant resources, expertise, and collaboration between researchers, clinicians, and industry partners.

Computer-assisted image processing is a medical term that refers to the use of computer systems and specialized software to improve, analyze, and interpret medical images obtained through various imaging techniques such as X-ray, CT (computed tomography), MRI (magnetic resonance imaging), ultrasound, and others.

The process typically involves several steps, including image acquisition, enhancement, segmentation, restoration, and analysis. Image processing algorithms can be used to enhance the quality of medical images by adjusting contrast, brightness, and sharpness, as well as removing noise and artifacts that may interfere with accurate diagnosis. Segmentation techniques can be used to isolate specific regions or structures of interest within an image, allowing for more detailed analysis.

Computer-assisted image processing has numerous applications in medical imaging, including detection and characterization of lesions, tumors, and other abnormalities; assessment of organ function and morphology; and guidance of interventional procedures such as biopsies and surgeries. By automating and standardizing image analysis tasks, computer-assisted image processing can help to improve diagnostic accuracy, efficiency, and consistency, while reducing the potential for human error.

A plant extract is a preparation containing chemical constituents that have been extracted from a plant using a solvent. The resulting extract may contain a single compound or a mixture of several compounds, depending on the extraction process and the specific plant material used. These extracts are often used in various industries including pharmaceuticals, nutraceuticals, cosmetics, and food and beverage, due to their potential therapeutic or beneficial properties. The composition of plant extracts can vary widely, and it is important to ensure their quality, safety, and efficacy before use in any application.

Solubility is a fundamental concept in pharmaceutical sciences and medicine, which refers to the maximum amount of a substance (solute) that can be dissolved in a given quantity of solvent (usually water) at a specific temperature and pressure. Solubility is typically expressed as mass of solute per volume or mass of solvent (e.g., grams per liter, milligrams per milliliter). The process of dissolving a solute in a solvent results in a homogeneous solution where the solute particles are dispersed uniformly throughout the solvent.

Understanding the solubility of drugs is crucial for their formulation, administration, and therapeutic effectiveness. Drugs with low solubility may not dissolve sufficiently to produce the desired pharmacological effect, while those with high solubility might lead to rapid absorption and short duration of action. Therefore, optimizing drug solubility through various techniques like particle size reduction, salt formation, or solubilization is an essential aspect of drug development and delivery.

Cell-and tissue-based therapy is a type of medical treatment that involves the use of living cells or tissues to repair, replace, or regenerate damaged or diseased cells or tissues in the body. This can include the transplantation of stem cells, which are immature cells that have the ability to develop into different types of cells, as well as the use of fully differentiated cells or tissues that have specific functions in the body.

Cell-and tissue-based therapies may be used to treat a wide variety of medical conditions, including degenerative diseases, injuries, and congenital defects. Some examples of cell-and tissue-based therapies include:

* Bone marrow transplantation: This involves the transplantation of blood-forming stem cells from the bone marrow of a healthy donor to a patient in need of new blood cells due to disease or treatment with chemotherapy or radiation.
* Corneal transplantation: This involves the transplantation of healthy corneal tissue from a deceased donor to a patient with damaged or diseased corneas.
* Articular cartilage repair: This involves the use of cells or tissues to repair damaged articular cartilage, which is the smooth, white tissue that covers the ends of bones where they come together to form joints.

Cell-and tissue-based therapies are a rapidly evolving field of medicine, and researchers are continually exploring new ways to use these treatments to improve patient outcomes. However, it is important to note that cell-and tissue-based therapies also carry some risks, including the possibility of rejection or infection, and they should only be performed by qualified medical professionals in appropriate settings.

Cerebrospinal fluid (CSF) proteins refer to the proteins present in the cerebrospinal fluid, which is a clear, colorless fluid that surrounds and protects the brain and spinal cord. The protein concentration in the CSF is much lower than that in the blood, and it contains a specific set of proteins that are produced by the brain, spinal cord, and associated tissues.

The normal range for CSF protein levels is typically between 15-45 mg/dL, although this can vary slightly depending on the laboratory's reference range. An elevation in CSF protein levels may indicate the presence of neurological disorders such as meningitis, encephalitis, multiple sclerosis, or Guillain-Barre syndrome. Additionally, certain conditions such as spinal cord injury, brain tumors, or neurodegenerative diseases can also cause an increase in CSF protein levels.

Therefore, measuring CSF protein levels is an important diagnostic tool for neurologists to evaluate various neurological disorders and monitor disease progression. However, it's essential to interpret the results of CSF protein tests in conjunction with other clinical findings and laboratory test results to make an accurate diagnosis.

Caspases are a family of protease enzymes that play essential roles in programmed cell death, also known as apoptosis. These enzymes are produced as inactive precursors and are activated when cells receive signals to undergo apoptosis. Once activated, caspases cleave specific protein substrates, leading to the characteristic morphological changes and DNA fragmentation associated with apoptotic cell death. Caspases also play roles in other cellular processes, including inflammation and differentiation. There are two types of caspases: initiator caspases (caspase-2, -8, -9, and -10) and effector caspases (caspase-3, -6, and -7). Initiator caspases are activated in response to various apoptotic signals and then activate the effector caspases, which carry out the proteolytic cleavage of cellular proteins. Dysregulation of caspase activity has been implicated in a variety of diseases, including neurodegenerative disorders, ischemic injury, and cancer.

Metabolic brain diseases refer to a group of conditions that are caused by disruptions in the body's metabolic processes, which affect the brain. These disorders can be inherited or acquired and can result from problems with the way the body produces, breaks down, or uses energy and nutrients.

Examples of metabolic brain diseases include:

1. Mitochondrial encephalomyopathies: These are a group of genetic disorders that affect the mitochondria, which are the energy-producing structures in cells. When the mitochondria don't function properly, it can lead to muscle weakness, neurological problems, and developmental delays.
2. Leukodystrophies: These are a group of genetic disorders that affect the white matter of the brain, which is made up of nerve fibers covered in myelin, a fatty substance that insulates the fibers and helps them transmit signals. When the myelin breaks down or is not produced properly, it can lead to cognitive decline, motor problems, and other neurological symptoms.
3. Lysosomal storage disorders: These are genetic disorders that affect the lysosomes, which are structures in cells that break down waste products and recycle cellular materials. When the lysosomes don't function properly, it can lead to the accumulation of waste products in cells, including brain cells, causing damage and neurological symptoms.
4. Maple syrup urine disease: This is a genetic disorder that affects the way the body breaks down certain amino acids, leading to a buildup of toxic levels of these substances in the blood and urine. If left untreated, it can cause brain damage, developmental delays, and other neurological problems.
5. Homocystinuria: This is a genetic disorder that affects the way the body processes an amino acid called methionine, leading to a buildup of homocysteine in the blood. High levels of homocysteine can cause damage to the blood vessels and lead to neurological problems, including seizures, developmental delays, and cognitive decline.

Treatment for metabolic brain diseases may involve dietary changes, supplements, medications, or other therapies aimed at managing symptoms and preventing further damage to the brain. In some cases, a stem cell transplant may be recommended as a treatment option.

Small interfering RNA (siRNA) is a type of short, double-stranded RNA molecule that plays a role in the RNA interference (RNAi) pathway. The RNAi pathway is a natural cellular process that regulates gene expression by targeting and destroying specific messenger RNA (mRNA) molecules, thereby preventing the translation of those mRNAs into proteins.

SiRNAs are typically 20-25 base pairs in length and are generated from longer double-stranded RNA precursors called hairpin RNAs or dsRNAs by an enzyme called Dicer. Once generated, siRNAs associate with a protein complex called the RNA-induced silencing complex (RISC), which uses one strand of the siRNA (the guide strand) to recognize and bind to complementary sequences in the target mRNA. The RISC then cleaves the target mRNA, leading to its degradation and the inhibition of protein synthesis.

SiRNAs have emerged as a powerful tool for studying gene function and have shown promise as therapeutic agents for a variety of diseases, including viral infections, cancer, and genetic disorders. However, their use as therapeutics is still in the early stages of development, and there are challenges associated with delivering siRNAs to specific cells and tissues in the body.

Gene expression profiling is a laboratory technique used to measure the activity (expression) of thousands of genes at once. This technique allows researchers and clinicians to identify which genes are turned on or off in a particular cell, tissue, or organism under specific conditions, such as during health, disease, development, or in response to various treatments.

The process typically involves isolating RNA from the cells or tissues of interest, converting it into complementary DNA (cDNA), and then using microarray or high-throughput sequencing technologies to determine which genes are expressed and at what levels. The resulting data can be used to identify patterns of gene expression that are associated with specific biological states or processes, providing valuable insights into the underlying molecular mechanisms of diseases and potential targets for therapeutic intervention.

In recent years, gene expression profiling has become an essential tool in various fields, including cancer research, drug discovery, and personalized medicine, where it is used to identify biomarkers of disease, predict patient outcomes, and guide treatment decisions.

Lysosomal storage diseases (LSDs) are a group of rare inherited metabolic disorders caused by defects in lysosomal function. Lysosomes are membrane-bound organelles within cells that contain enzymes responsible for breaking down and recycling various biomolecules, such as proteins, lipids, and carbohydrates. In LSDs, the absence or deficiency of specific lysosomal enzymes leads to the accumulation of undigested substrates within the lysosomes, resulting in cellular dysfunction and organ damage.

These disorders can affect various organs and systems in the body, including the brain, nervous system, bones, skin, and visceral organs. Symptoms may include developmental delays, neurological impairment, motor dysfunction, bone abnormalities, coarse facial features, hepatosplenomegaly (enlarged liver and spleen), and recurrent infections.

Examples of LSDs include Gaucher disease, Tay-Sachs disease, Niemann-Pick disease, Fabry disease, Pompe disease, and mucopolysaccharidoses (MPS). Treatment options for LSDs may include enzyme replacement therapy, substrate reduction therapy, or bone marrow transplantation. Early diagnosis and intervention can help improve the prognosis and quality of life for affected individuals.

RNA-binding proteins (RBPs) are a class of proteins that selectively interact with RNA molecules to form ribonucleoprotein complexes. These proteins play crucial roles in the post-transcriptional regulation of gene expression, including pre-mRNA processing, mRNA stability, transport, localization, and translation. RBPs recognize specific RNA sequences or structures through their modular RNA-binding domains, which can be highly degenerate and allow for the recognition of a wide range of RNA targets. The interaction between RBPs and RNA is often dynamic and can be regulated by various post-translational modifications of the proteins or by environmental stimuli, allowing for fine-tuning of gene expression in response to changing cellular needs. Dysregulation of RBP function has been implicated in various human diseases, including neurological disorders and cancer.

Methylazoxymethanol Acetate (MAM) is not a medication or therapeutic agent used in human medicine. It is a research tool, specifically a neurotoxin, that is used in laboratory studies to help understand the development and organization of the nervous system, particularly in relation to neurodegenerative disorders and brain injuries.

MAM is primarily used in animal models, often rats or mice, to study the effects of early life exposure to neurotoxic substances on brain development. It is known to cause widespread degeneration of nerve cells (neurons) and disruption of normal neural connections, which can provide valuable insights into the processes underlying various neurological conditions.

However, it's important to note that MAM is not used as a treatment or therapy in human medicine due to its neurotoxic properties.

Aldehydes are a class of organic compounds characterized by the presence of a functional group consisting of a carbon atom bonded to a hydrogen atom and a double bonded oxygen atom, also known as a formyl or aldehyde group. The general chemical structure of an aldehyde is R-CHO, where R represents a hydrocarbon chain.

Aldehydes are important in biochemistry and medicine as they are involved in various metabolic processes and are found in many biological molecules. For example, glucose is converted to pyruvate through a series of reactions that involve aldehyde intermediates. Additionally, some aldehydes have been identified as toxicants or environmental pollutants, such as formaldehyde, which is a known carcinogen and respiratory irritant.

Formaldehyde is also commonly used in medical and laboratory settings for its disinfectant properties and as a fixative for tissue samples. However, exposure to high levels of formaldehyde can be harmful to human health, causing symptoms such as coughing, wheezing, and irritation of the eyes, nose, and throat. Therefore, appropriate safety measures must be taken when handling aldehydes in medical and laboratory settings.

Medical Definition of "Multiprotein Complexes" :

Multiprotein complexes are large molecular assemblies composed of two or more proteins that interact with each other to carry out specific cellular functions. These complexes can range from relatively simple dimers or trimers to massive structures containing hundreds of individual protein subunits. They are formed through a process known as protein-protein interaction, which is mediated by specialized regions on the protein surface called domains or motifs.

Multiprotein complexes play critical roles in many cellular processes, including signal transduction, gene regulation, DNA replication and repair, protein folding and degradation, and intracellular transport. The formation of these complexes is often dynamic and regulated in response to various stimuli, allowing for precise control of their function.

Disruption of multiprotein complexes can lead to a variety of diseases, including cancer, neurodegenerative disorders, and infectious diseases. Therefore, understanding the structure, composition, and regulation of these complexes is an important area of research in molecular biology and medicine.

A transgene is a segment of DNA that has been artificially transferred from one organism to another, typically between different species, to introduce a new trait or characteristic. The term "transgene" specifically refers to the genetic material that has been transferred and has become integrated into the host organism's genome. This technology is often used in genetic engineering and biomedical research, including the development of genetically modified organisms (GMOs) for agricultural purposes or the creation of animal models for studying human diseases.

Transgenes can be created using various techniques, such as molecular cloning, where a desired gene is isolated, manipulated, and then inserted into a vector (a small DNA molecule, such as a plasmid) that can efficiently enter the host organism's cells. Once inside the cell, the transgene can integrate into the host genome, allowing for the expression of the new trait in the resulting transgenic organism.

It is important to note that while transgenes can provide valuable insights and benefits in research and agriculture, their use and release into the environment are subjects of ongoing debate due to concerns about potential ecological impacts and human health risks.

Enzyme activation refers to the process by which an enzyme becomes biologically active and capable of carrying out its specific chemical or biological reaction. This is often achieved through various post-translational modifications, such as proteolytic cleavage, phosphorylation, or addition of cofactors or prosthetic groups to the enzyme molecule. These modifications can change the conformation or structure of the enzyme, exposing or creating a binding site for the substrate and allowing the enzymatic reaction to occur.

For example, in the case of proteolytic cleavage, an inactive precursor enzyme, known as a zymogen, is cleaved into its active form by a specific protease. This is seen in enzymes such as trypsin and chymotrypsin, which are initially produced in the pancreas as inactive precursors called trypsinogen and chymotrypsinogen, respectively. Once they reach the small intestine, they are activated by enteropeptidase, a protease that cleaves a specific peptide bond, releasing the active enzyme.

Phosphorylation is another common mechanism of enzyme activation, where a phosphate group is added to a specific serine, threonine, or tyrosine residue on the enzyme by a protein kinase. This modification can alter the conformation of the enzyme and create a binding site for the substrate, allowing the enzymatic reaction to occur.

Enzyme activation is a crucial process in many biological pathways, as it allows for precise control over when and where specific reactions take place. It also provides a mechanism for regulating enzyme activity in response to various signals and stimuli, such as hormones, neurotransmitters, or changes in the intracellular environment.

Mass spectrometry (MS) is an analytical technique used to identify and quantify the chemical components of a mixture or compound. It works by ionizing the sample, generating charged molecules or fragments, and then measuring their mass-to-charge ratio in a vacuum. The resulting mass spectrum provides information about the molecular weight and structure of the analytes, allowing for identification and characterization.

In simpler terms, mass spectrometry is a method used to determine what chemicals are present in a sample and in what quantities, by converting the chemicals into ions, measuring their masses, and generating a spectrum that shows the relative abundances of each ion type.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

According to the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), an Adjustment Disorder is a mental health condition that occurs as a reaction to a stressful life event or significant change. It is characterized by emotional or behavioral symptoms that cause distress and interfere with daily functioning, but do not meet the criteria for other more specific mental disorders.

The symptoms of an Adjustment Disorder typically develop within three months of the identified stressor and may include:

* Depressed mood
* Anxiety
* Irritability or anger
* Worrying
* Difficulty sleeping
* Loss of appetite
* Difficulty concentrating
* Physical symptoms, such as headaches or stomachaches

The symptoms must be out of proportion to the severity or intensity of the stressor and may lead to significant impairment in social, occupational, or academic functioning. The diagnosis is not given if the symptoms persist for more than six months after the stressor has ended.

There are several subtypes of Adjustment Disorders, including:

* Adjustment Disorder with Depressed Mood
* Adjustment Disorder with Anxiety
* Adjustment Disorder with Mixed Anxiety and Depressed Mood
* Adjustment Disorder with Disturbance of Conduct
* Adjustment Disorder with Emotional or Behavioral Symptoms Not Otherwise Specified

Treatment for Adjustment Disorders typically involves psychotherapy, such as cognitive-behavioral therapy (CBT) or solution-focused brief therapy, to help individuals develop coping skills and manage their symptoms. In some cases, medication may also be recommended to alleviate symptoms of anxiety or depression.

Congo Red is a synthetic diazo dye that is commonly used in histology and pathology for stainings and tests. It is particularly useful in identifying amyloid deposits in tissues, which are associated with various diseases such as Alzheimer's disease, type 2 diabetes, and systemic amyloidosis.

When Congo Red binds to amyloid fibrils, it exhibits a characteristic apple-green birefringence under polarized light microscopy. Additionally, Congo Red stained amyloid deposits show a shift in their emission spectrum when excited with circularly polarized light, a phenomenon known as dichroism. These properties make Congo Red a valuable tool for the diagnosis and study of amyloidosis and other protein misfolding disorders.

It is important to note that Congo Red staining should be performed with care, as it can be toxic and carcinogenic if not handled properly.

Sandhoff disease is a rare inherited disorder that affects the nervous system. It's a type of GM2 gangliosidosis, which is a group of conditions characterized by the body's inability to break down certain fats (lipids) called gangliosides.

In Sandhoff disease, deficiencies in the enzymes hexosaminidase A and B lead to an accumulation of GM2 ganglioside in various cells, particularly in nerve cells of the brain. This accumulation results in progressive damage to the nervous system.

The symptoms of Sandhoff disease typically appear between 6 months and 2 years of age and can include developmental delay, seizures, an exaggerated startle response, muscle weakness, loss of motor skills, and vision and hearing loss. The condition is often fatal by around age 3. It's caused by mutations in the HEXB gene, and it's inherited in an autosomal recessive manner, meaning an individual must inherit two copies of the mutated gene (one from each parent) to develop the disease.

Retinal degeneration is a broad term that refers to the progressive loss of photoreceptor cells (rods and cones) in the retina, which are responsible for converting light into electrical signals that are sent to the brain. This process can lead to vision loss or blindness. There are many different types of retinal degeneration, including age-related macular degeneration, retinitis pigmentosa, and Stargardt's disease, among others. These conditions can have varying causes, such as genetic mutations, environmental factors, or a combination of both. Treatment options vary depending on the specific type and progression of the condition.

Caspase-12 is a type of protease enzyme that belongs to the family of caspases, which are cysteine-aspartic acid proteases playing essential roles in programmed cell death (apoptosis). Caspase-12 is primarily expressed in the endoplasmic reticulum (ER) and is involved in ER stress-induced apoptosis.

During ER stress, misfolded or unfolded proteins accumulate in the ER lumen, triggering an adaptive response called the unfolded protein response (UPR). If the UPR fails to restore ER homeostasis, caspase-12 is activated and contributes to the initiation of the apoptotic process.

However, it's worth noting that the role of caspase-12 in human apoptosis remains controversial, as some studies suggest its function might be limited or absent in humans compared to other species like mice.

Glaucoma is a group of eye conditions that damage the optic nerve, often caused by an abnormally high pressure in the eye (intraocular pressure). This damage can lead to permanent vision loss or even blindness if left untreated. The most common type is open-angle glaucoma, which has no warning signs and progresses slowly. Angle-closure glaucoma, on the other hand, can cause sudden eye pain, redness, nausea, and vomiting, as well as rapid vision loss. Other less common types of glaucoma also exist. While there is no cure for glaucoma, early detection and treatment can help slow or prevent further vision loss.

Neuronal plasticity, also known as neuroplasticity or neural plasticity, refers to the ability of the brain and nervous system to change and adapt as a result of experience, learning, injury, or disease. This can involve changes in the structure, organization, and function of neurons (nerve cells) and their connections (synapses) in the central and peripheral nervous systems.

Neuronal plasticity can take many forms, including:

* Synaptic plasticity: Changes in the strength or efficiency of synaptic connections between neurons. This can involve the formation, elimination, or modification of synapses.
* Neural circuit plasticity: Changes in the organization and connectivity of neural circuits, which are networks of interconnected neurons that process information.
* Structural plasticity: Changes in the physical structure of neurons, such as the growth or retraction of dendrites (branches that receive input from other neurons) or axons (projections that transmit signals to other neurons).
* Functional plasticity: Changes in the physiological properties of neurons, such as their excitability, responsiveness, or sensitivity to stimuli.

Neuronal plasticity is a fundamental property of the nervous system and plays a crucial role in many aspects of brain function, including learning, memory, perception, and cognition. It also contributes to the brain's ability to recover from injury or disease, such as stroke or traumatic brain injury.

Immunoblotting, also known as western blotting, is a laboratory technique used in molecular biology and immunogenetics to detect and quantify specific proteins in a complex mixture. This technique combines the electrophoretic separation of proteins by gel electrophoresis with their detection using antibodies that recognize specific epitopes (protein fragments) on the target protein.

The process involves several steps: first, the protein sample is separated based on size through sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Next, the separated proteins are transferred onto a nitrocellulose or polyvinylidene fluoride (PVDF) membrane using an electric field. The membrane is then blocked with a blocking agent to prevent non-specific binding of antibodies.

After blocking, the membrane is incubated with a primary antibody that specifically recognizes the target protein. Following this, the membrane is washed to remove unbound primary antibodies and then incubated with a secondary antibody conjugated to an enzyme such as horseradish peroxidase (HRP) or alkaline phosphatase (AP). The enzyme catalyzes a colorimetric or chemiluminescent reaction that allows for the detection of the target protein.

Immunoblotting is widely used in research and clinical settings to study protein expression, post-translational modifications, protein-protein interactions, and disease biomarkers. It provides high specificity and sensitivity, making it a valuable tool for identifying and quantifying proteins in various biological samples.

Nitric oxide (NO) is a molecule made up of one nitrogen atom and one oxygen atom. In the body, it is a crucial signaling molecule involved in various physiological processes such as vasodilation, immune response, neurotransmission, and inhibition of platelet aggregation. It is produced naturally by the enzyme nitric oxide synthase (NOS) from the amino acid L-arginine. Inhaled nitric oxide is used medically to treat pulmonary hypertension in newborns and adults, as it helps to relax and widen blood vessels, improving oxygenation and blood flow.

An autopsy, also known as a post-mortem examination or obduction, is a medical procedure in which a qualified professional (usually a pathologist) examines a deceased person's body to determine the cause and manner of death. This process may involve various investigative techniques, such as incisions to study internal organs, tissue sampling, microscopic examination, toxicology testing, and other laboratory analyses. The primary purpose of an autopsy is to gather objective evidence about the medical conditions and factors contributing to the individual's demise, which can be essential for legal, insurance, or public health purposes. Additionally, autopsies can provide valuable insights into disease processes and aid in advancing medical knowledge.

I must clarify that the term "pedigree" is not typically used in medical definitions. Instead, it is often employed in genetics and breeding, where it refers to the recorded ancestry of an individual or a family, tracing the inheritance of specific traits or diseases. In human genetics, a pedigree can help illustrate the pattern of genetic inheritance in families over multiple generations. However, it is not a medical term with a specific clinical definition.

Cytoplasm is the material within a eukaryotic cell (a cell with a true nucleus) that lies between the nuclear membrane and the cell membrane. It is composed of an aqueous solution called cytosol, in which various organelles such as mitochondria, ribosomes, endoplasmic reticulum, Golgi apparatus, lysosomes, and vacuoles are suspended. Cytoplasm also contains a variety of dissolved nutrients, metabolites, ions, and enzymes that are involved in various cellular processes such as metabolism, signaling, and transport. It is where most of the cell's metabolic activities take place, and it plays a crucial role in maintaining the structure and function of the cell.

Lipopolysaccharides (LPS) are large molecules found in the outer membrane of Gram-negative bacteria. They consist of a hydrophilic polysaccharide called the O-antigen, a core oligosaccharide, and a lipid portion known as Lipid A. The Lipid A component is responsible for the endotoxic activity of LPS, which can trigger a powerful immune response in animals, including humans. This response can lead to symptoms such as fever, inflammation, and septic shock, especially when large amounts of LPS are introduced into the bloodstream.

Endopeptidase K is a type of enzyme that belongs to the family of peptidases, which are proteins that help break down other proteins into smaller molecules called peptides or individual amino acids. Specifically, endopeptidase K is an intracellular serine protease that cleaves peptide bonds within a protein's interior, rather than at its ends.

Endopeptidase K was initially identified as a component of the proteasome, a large protein complex found in the nucleus and cytoplasm of eukaryotic cells. The proteasome plays a critical role in regulating protein turnover and degrading damaged or misfolded proteins. Endopeptidase K is one of several enzymes that make up the proteasome's catalytic core, where it helps cleave proteins into smaller peptides for further processing and eventual destruction.

Endopeptidase K has also been found to be involved in other cellular processes, such as regulating the activity of certain signaling molecules and contributing to the immune response. However, its precise functions and substrates are still being studied and elucidated.

"Age factors" refer to the effects, changes, or differences that age can have on various aspects of health, disease, and medical care. These factors can encompass a wide range of issues, including:

1. Physiological changes: As people age, their bodies undergo numerous physical changes that can affect how they respond to medications, illnesses, and medical procedures. For example, older adults may be more sensitive to certain drugs or have weaker immune systems, making them more susceptible to infections.
2. Chronic conditions: Age is a significant risk factor for many chronic diseases, such as heart disease, diabetes, cancer, and arthritis. As a result, age-related medical issues are common and can impact treatment decisions and outcomes.
3. Cognitive decline: Aging can also lead to cognitive changes, including memory loss and decreased decision-making abilities. These changes can affect a person's ability to understand and comply with medical instructions, leading to potential complications in their care.
4. Functional limitations: Older adults may experience physical limitations that impact their mobility, strength, and balance, increasing the risk of falls and other injuries. These limitations can also make it more challenging for them to perform daily activities, such as bathing, dressing, or cooking.
5. Social determinants: Age-related factors, such as social isolation, poverty, and lack of access to transportation, can impact a person's ability to obtain necessary medical care and affect their overall health outcomes.

Understanding age factors is critical for healthcare providers to deliver high-quality, patient-centered care that addresses the unique needs and challenges of older adults. By taking these factors into account, healthcare providers can develop personalized treatment plans that consider a person's age, physical condition, cognitive abilities, and social circumstances.

'Cercopithecus aethiops' is the scientific name for the monkey species more commonly known as the green monkey. It belongs to the family Cercopithecidae and is native to western Africa. The green monkey is omnivorous, with a diet that includes fruits, nuts, seeds, insects, and small vertebrates. They are known for their distinctive greenish-brown fur and long tail. Green monkeys are also important animal models in biomedical research due to their susceptibility to certain diseases, such as SIV (simian immunodeficiency virus), which is closely related to HIV.

Nootropic agents, also known as cognition enhancers or smart drugs, are substances that are believed to improve cognitive functions such as memory, motivation, creativity, and executive functions. The term "nootropic" is derived from the Greek words "nous," meaning mind, and "tropos," meaning a turn or bend.

Nootropics can be divided into several categories, including dietary supplements, prescription medications, and illicit substances. Some examples of nootropics include:

* Piracetam and other racetams
* Caffeine and other stimulants
* Nicotine and other cholinergic compounds
* Modafinil and other wakefulness-promoting agents
* Certain antidepressants, such as fluoxetine and bupropion
* Illicit substances, such as methylphenidate (Ritalin) and amphetamines (Adderall), which are sometimes used off-label for cognitive enhancement.

It is important to note that while some nootropic agents have been shown to have cognitive benefits in certain studies, their effectiveness and safety are not fully understood. Additionally, the long-term use of some nootropics can have potential risks and side effects. Therefore, it is recommended to consult with a healthcare professional before starting any new supplement or medication regimen for cognitive enhancement.

Galactosylceramidase (galactocerebrosidase) is an enzyme that breaks down a fatty substance called galactosylceramide, which is found in myelin – the protective covering of nerve fibers in the brain. This enzyme plays a crucial role in the maintenance and functioning of the nervous system.

Deficiency of galactosylceramidase leads to the accumulation of galactosylceramide in the lysosomes (membrane-bound organelles responsible for breaking down waste materials within cells), resulting in an inherited metabolic disorder known as Krabbe disease or globoid cell leukodystrophy. This rare and progressive neurological condition affects the development and maintenance of myelin, causing severe damage to the nervous system and leading to motor, cognitive, and sensory impairments, ultimately resulting in early death if left untreated.

Recombinant fusion proteins are artificially created biomolecules that combine the functional domains or properties of two or more different proteins into a single protein entity. They are generated through recombinant DNA technology, where the genes encoding the desired protein domains are linked together and expressed as a single, chimeric gene in a host organism, such as bacteria, yeast, or mammalian cells.

The resulting fusion protein retains the functional properties of its individual constituent proteins, allowing for novel applications in research, diagnostics, and therapeutics. For instance, recombinant fusion proteins can be designed to enhance protein stability, solubility, or immunogenicity, making them valuable tools for studying protein-protein interactions, developing targeted therapies, or generating vaccines against infectious diseases or cancer.

Examples of recombinant fusion proteins include:

1. Etaglunatide (ABT-523): A soluble Fc fusion protein that combines the heavy chain fragment crystallizable region (Fc) of an immunoglobulin with the extracellular domain of the human interleukin-6 receptor (IL-6R). This fusion protein functions as a decoy receptor, neutralizing IL-6 and its downstream signaling pathways in rheumatoid arthritis.
2. Etanercept (Enbrel): A soluble TNF receptor p75 Fc fusion protein that binds to tumor necrosis factor-alpha (TNF-α) and inhibits its proinflammatory activity, making it a valuable therapeutic option for treating autoimmune diseases like rheumatoid arthritis, ankylosing spondylitis, and psoriasis.
3. Abatacept (Orencia): A fusion protein consisting of the extracellular domain of cytotoxic T-lymphocyte antigen 4 (CTLA-4) linked to the Fc region of an immunoglobulin, which downregulates T-cell activation and proliferation in autoimmune diseases like rheumatoid arthritis.
4. Belimumab (Benlysta): A monoclonal antibody that targets B-lymphocyte stimulator (BLyS) protein, preventing its interaction with the B-cell surface receptor and inhibiting B-cell activation in systemic lupus erythematosus (SLE).
5. Romiplostim (Nplate): A fusion protein consisting of a thrombopoietin receptor agonist peptide linked to an immunoglobulin Fc region, which stimulates platelet production in patients with chronic immune thrombocytopenia (ITP).
6. Darbepoetin alfa (Aranesp): A hyperglycosylated erythropoiesis-stimulating protein that functions as a longer-acting form of recombinant human erythropoietin, used to treat anemia in patients with chronic kidney disease or cancer.
7. Palivizumab (Synagis): A monoclonal antibody directed against the F protein of respiratory syncytial virus (RSV), which prevents RSV infection and is administered prophylactically to high-risk infants during the RSV season.
8. Ranibizumab (Lucentis): A recombinant humanized monoclonal antibody fragment that binds and inhibits vascular endothelial growth factor A (VEGF-A), used in the treatment of age-related macular degeneration, diabetic retinopathy, and other ocular disorders.
9. Cetuximab (Erbitux): A chimeric monoclonal antibody that binds to epidermal growth factor receptor (EGFR), used in the treatment of colorectal cancer and head and neck squamous cell carcinoma.
10. Adalimumab (Humira): A fully humanized monoclonal antibody that targets tumor necrosis factor-alpha (TNF-α), used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriasis, and Crohn's disease.
11. Bevacizumab (Avastin): A recombinant humanized monoclonal antibody that binds to VEGF-A, used in the treatment of various cancers, including colorectal, lung, breast, and kidney cancer.
12. Trastuzumab (Herceptin): A humanized monoclonal antibody that targets HER2/neu receptor, used in the treatment of breast cancer.
13. Rituximab (Rituxan): A chimeric monoclonal antibody that binds to CD20 antigen on B cells, used in the treatment of non-Hodgkin's lymphoma and rheumatoid arthritis.
14. Palivizumab (Synagis): A humanized monoclonal antibody that binds to the F protein of respiratory syncytial virus, used in the prevention of respiratory syncytial virus infection in high-risk infants.
15. Infliximab (Remicade): A chimeric monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including Crohn's disease, ulcerative colitis, rheumatoid arthritis, and ankylosing spondylitis.
16. Natalizumab (Tysabri): A humanized monoclonal antibody that binds to α4β1 integrin, used in the treatment of multiple sclerosis and Crohn's disease.
17. Adalimumab (Humira): A fully human monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn's disease, and ulcerative colitis.
18. Golimumab (Simponi): A fully human monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and ulcerative colitis.
19. Certolizumab pegol (Cimzia): A PEGylated Fab' fragment of a humanized monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease.
20. Ustekinumab (Stelara): A fully human monoclonal antibody that targets IL-12 and IL-23, used in the treatment of psoriasis, psoriatic arthritis, and Crohn's disease.
21. Secukinumab (Cosentyx): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis, psoriatic arthritis, and ankylosing spondylitis.
22. Ixekizumab (Taltz): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis and psoriatic arthritis.
23. Brodalumab (Siliq): A fully human monoclonal antibody that targets IL-17 receptor A, used in the treatment of psoriasis.
24. Sarilumab (Kevzara): A fully human monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis.
25. Tocilizumab (Actemra): A humanized monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis, systemic juvenile idiopathic arthritis, polyarticular juvenile idiopathic arthritis, giant cell arteritis, and chimeric antigen receptor T-cell-induced cytokine release syndrome.
26. Siltuximab (Sylvant): A chimeric monoclonal antibody that targets IL-6, used in the treatment of multicentric Castleman disease.
27. Satralizumab (Enspryng): A humanized monoclonal antibody that targets IL-6 receptor alpha, used in the treatment of neuromyelitis optica spectrum disorder.
28. Sirukumab (Plivensia): A human monoclonal antibody that targets IL-6, used in the treatment

Gerstmann-Straussler-Scheinker disease (GSS) is a rare, inherited, progressive neurodegenerative disorder characterized by cerebellar ataxia, pyramidal signs, and distinctive histopathological features in the brain. It is caused by mutations in the PRNP gene, which encodes the prion protein. The disease is transmitted in an autosomal dominant pattern, meaning that a single copy of the mutated gene from either parent is sufficient to cause the disorder.

GSS typically begins in mid-adulthood and progresses over several years to a decade, leading to severe disability and death. The symptoms of GSS include cerebellar ataxia (difficulty with coordination and balance), pyramidal signs (stiffness, spasticity, and hyperreflexia in the limbs), and various other neurological features such as dementia, visual disturbances, and speech difficulties.

Histopathologically, GSS is characterized by the accumulation of abnormal prion protein aggregates in the brain, which can be detected using special staining techniques. These aggregates are thought to be responsible for the neurodegeneration and clinical symptoms of the disease. Currently, there is no cure for GSS and treatment is focused on managing the symptoms of the disorder.

Lysosome-Associated Membrane Protein 2 (LAMP-2) is a type of transmembrane protein that is primarily found in the membranes of lysosomes, which are organelles within cells responsible for breaking down and recycling various cellular components. LAMP-2 plays a crucial role in maintaining the structural integrity and stability of the lysosomal membrane. It also participates in the process of autophagy, where damaged or unnecessary cellular components are engulfed by membranes to form vesicles called autophagosomes, which then fuse with lysosomes for degradation. Mutations in the LAMP-2 gene have been associated with certain genetic disorders, such as Danon disease, a rare X-linked condition characterized by heart problems, muscle weakness, and intellectual disability.

Synaptic transmission is the process by which a neuron communicates with another cell, such as another neuron or a muscle cell, across a junction called a synapse. It involves the release of neurotransmitters from the presynaptic terminal of the neuron, which then cross the synaptic cleft and bind to receptors on the postsynaptic cell, leading to changes in the electrical or chemical properties of the target cell. This process is critical for the transmission of signals within the nervous system and for controlling various physiological functions in the body.

Genotype, in genetics, refers to the complete heritable genetic makeup of an individual organism, including all of its genes. It is the set of instructions contained in an organism's DNA for the development and function of that organism. The genotype is the basis for an individual's inherited traits, and it can be contrasted with an individual's phenotype, which refers to the observable physical or biochemical characteristics of an organism that result from the expression of its genes in combination with environmental influences.

It is important to note that an individual's genotype is not necessarily identical to their genetic sequence. Some genes have multiple forms called alleles, and an individual may inherit different alleles for a given gene from each parent. The combination of alleles that an individual inherits for a particular gene is known as their genotype for that gene.

Understanding an individual's genotype can provide important information about their susceptibility to certain diseases, their response to drugs and other treatments, and their risk of passing on inherited genetic disorders to their offspring.

An animal model in medicine refers to the use of non-human animals in experiments to understand, predict, and test responses and effects of various biological and chemical interactions that may also occur in humans. These models are used when studying complex systems or processes that cannot be easily replicated or studied in human subjects, such as genetic manipulation or exposure to harmful substances. The choice of animal model depends on the specific research question being asked and the similarities between the animal's and human's biological and physiological responses. Examples of commonly used animal models include mice, rats, rabbits, guinea pigs, and non-human primates.

Metabolic Flux Analysis (MFA) is not a medical term, but rather a term used in biochemistry and molecular biology. It refers to a mathematical modeling approach used to quantify the flow rates of metabolites through metabolic pathways in biological systems, such as cells or organisms. MFA uses measured data on the consumption and production rates of metabolites, along with knowledge of the reactions that make up the metabolic network, to estimate the fluxes (rates of reaction) through each pathway. This approach can help elucidate the regulation and dynamics of metabolic networks in response to genetic or environmental perturbations, and has applications in fields such as metabolic engineering and systems biology.

A Small Molecule Library is a collection of a large number of chemically synthesized, low molecular weight (typically under 900 daltons) compounds, which are used in drug discovery and development research. These libraries contain diverse structures and chemical properties, allowing researchers to screen them against specific targets, such as proteins or genes, to identify potential lead compounds that can be further optimized for therapeutic use. The use of small molecule libraries enables high-throughput screening, which is a rapid and efficient method to identify potential drug candidates.

Synaptophysin is a protein found in the presynaptic vesicles of neurons, which are involved in the release of neurotransmitters during synaptic transmission. It is often used as a marker for neuronal differentiation and is widely expressed in neuroendocrine cells and tumors. Synaptophysin plays a role in the regulation of neurotransmitter release and has been implicated in various neurological disorders, including Alzheimer's disease and synaptic dysfunction-related conditions.

A brain injury is defined as damage to the brain that occurs following an external force or trauma, such as a blow to the head, a fall, or a motor vehicle accident. Brain injuries can also result from internal conditions, such as lack of oxygen or a stroke. There are two main types of brain injuries: traumatic and acquired.

Traumatic brain injury (TBI) is caused by an external force that results in the brain moving within the skull or the skull being fractured. Mild TBIs may result in temporary symptoms such as headaches, confusion, and memory loss, while severe TBIs can cause long-term complications, including physical, cognitive, and emotional impairments.

Acquired brain injury (ABI) is any injury to the brain that occurs after birth and is not hereditary, congenital, or degenerative. ABIs are often caused by medical conditions such as strokes, tumors, anoxia (lack of oxygen), or infections.

Both TBIs and ABIs can range from mild to severe and may result in a variety of physical, cognitive, and emotional symptoms that can impact a person's ability to perform daily activities and function independently. Treatment for brain injuries typically involves a multidisciplinary approach, including medical management, rehabilitation, and supportive care.

N-Methyl-D-Aspartate (NMDA) is not a medication but a type of receptor, specifically a glutamate receptor, found in the post-synaptic membrane in the central nervous system. Glutamate is a major excitatory neurotransmitter in the brain. NMDA receptors are involved in various functions such as synaptic plasticity, learning, and memory. They also play a role in certain neurological disorders like epilepsy, neurodegenerative diseases, and chronic pain.

NMDA receptors are named after N-Methyl-D-Aspartate, a synthetic analog of the amino acid aspartic acid, which is a selective agonist for this type of receptor. An agonist is a substance that binds to a receptor and causes a response similar to that of the natural ligand (in this case, glutamate).

An allele is a variant form of a gene that is located at a specific position on a specific chromosome. Alleles are alternative forms of the same gene that arise by mutation and are found at the same locus or position on homologous chromosomes.

Each person typically inherits two copies of each gene, one from each parent. If the two alleles are identical, a person is said to be homozygous for that trait. If the alleles are different, the person is heterozygous.

For example, the ABO blood group system has three alleles, A, B, and O, which determine a person's blood type. If a person inherits two A alleles, they will have type A blood; if they inherit one A and one B allele, they will have type AB blood; if they inherit two B alleles, they will have type B blood; and if they inherit two O alleles, they will have type O blood.

Alleles can also influence traits such as eye color, hair color, height, and other physical characteristics. Some alleles are dominant, meaning that only one copy of the allele is needed to express the trait, while others are recessive, meaning that two copies of the allele are needed to express the trait.

Polyphenols are a type of phytochemical, which are naturally occurring compounds found in plant-based foods. They contain multiple phenol units and can be classified into several subgroups, including flavonoids, stilbenes, tannins, and lignans. These compounds have been studied for their potential health benefits due to their antioxidant, anti-inflammatory, and immune-modulating properties. They are found in a wide variety of foods such as fruits, vegetables, tea, wine, chocolate, and cereals.

The retina is the innermost, light-sensitive layer of tissue in the eye of many vertebrates and some cephalopods. It receives light that has been focused by the cornea and lens, converts it into neural signals, and sends these to the brain via the optic nerve. The retina contains several types of photoreceptor cells including rods (which handle vision in low light) and cones (which are active in bright light and are capable of color vision).

In medical terms, any pathological changes or diseases affecting the retinal structure and function can lead to visual impairment or blindness. Examples include age-related macular degeneration, diabetic retinopathy, retinal detachment, and retinitis pigmentosa among others.

Globoid cell leukodystrophy, also known as Krabbe disease, is a rare inherited disorder that affects the nervous system. It is characterized by the accumulation of abnormal quantities of a protein called psychosine in the brain's nerve cells, leading to their destruction and progressive damage to the protective sheath (myelin) that covers the nerves.

The term "leukodystrophy" refers to a group of disorders that affect the white matter of the brain, which is primarily composed of myelin. In globoid cell leukodystrophy, the accumulation of psychosine in the brain's nerve cells, particularly in macrophages (which are then referred to as "globoid cells"), results in progressive demyelination and severe neurological symptoms.

Early-onset forms of Krabbe disease typically present within the first six months of life, with symptoms such as irritability, feeding difficulties, muscle weakness, and developmental delays. Late-onset forms may not become apparent until later in childhood or even adulthood, with symptoms that can include vision loss, hearing impairment, muscle stiffness, and difficulty coordinating movements. The progression of the disease is often rapid, leading to severe disability and a shortened lifespan.

There is currently no cure for globoid cell leukodystrophy, but various treatments, such as bone marrow transplantation and enzyme replacement therapy, are being investigated to help manage the symptoms and slow down the progression of the disease.

The frontal lobe is the largest lobes of the human brain, located at the front part of each cerebral hemisphere and situated in front of the parietal and temporal lobes. It plays a crucial role in higher cognitive functions such as decision making, problem solving, planning, parts of social behavior, emotional expressions, physical reactions, and motor function. The frontal lobe is also responsible for what's known as "executive functions," which include the ability to focus attention, understand rules, switch focus, plan actions, and inhibit inappropriate behaviors. It is divided into five areas, each with its own specific functions: the primary motor cortex, premotor cortex, Broca's area, prefrontal cortex, and orbitofrontal cortex. Damage to the frontal lobe can result in a wide range of impairments, depending on the location and extent of the injury.

Atomic Force Microscopy (AFM) is a type of microscopy that allows visualization and measurement of surfaces at the atomic level. It works by using a sharp probe, called a tip, that is mounted on a flexible cantilever. The tip is brought very close to the surface of the sample and as the sample is scanned, the forces between the tip and the sample cause the cantilever to deflect. This deflection is measured and used to generate a topographic map of the surface with extremely high resolution, often on the order of fractions of a nanometer. AFM can be used to study both conductive and non-conductive samples, and can operate in various environments, including air and liquid. It has applications in fields such as materials science, biology, and chemistry.

Cell proliferation is the process by which cells increase in number, typically through the process of cell division. In the context of biology and medicine, it refers to the reproduction of cells that makes up living tissue, allowing growth, maintenance, and repair. It involves several stages including the transition from a phase of quiescence (G0 phase) to an active phase (G1 phase), DNA replication in the S phase, and mitosis or M phase, where the cell divides into two daughter cells.

Abnormal or uncontrolled cell proliferation is a characteristic feature of many diseases, including cancer, where deregulated cell cycle control leads to excessive and unregulated growth of cells, forming tumors that can invade surrounding tissues and metastasize to distant sites in the body.

Anti-inflammatory agents are a class of drugs or substances that reduce inflammation in the body. They work by inhibiting the production of inflammatory mediators, such as prostaglandins and leukotrienes, which are released during an immune response and contribute to symptoms like pain, swelling, redness, and warmth.

There are two main types of anti-inflammatory agents: steroidal and nonsteroidal. Steroidal anti-inflammatory drugs (SAIDs) include corticosteroids, which mimic the effects of hormones produced by the adrenal gland. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a larger group that includes both prescription and over-the-counter medications, such as aspirin, ibuprofen, naproxen, and celecoxib.

While both types of anti-inflammatory agents can be effective in reducing inflammation and relieving symptoms, they differ in their mechanisms of action, side effects, and potential risks. Long-term use of NSAIDs, for example, can increase the risk of gastrointestinal bleeding, kidney damage, and cardiovascular events. Corticosteroids can have significant side effects as well, particularly with long-term use, including weight gain, mood changes, and increased susceptibility to infections.

It's important to use anti-inflammatory agents only as directed by a healthcare provider, and to be aware of potential risks and interactions with other medications or health conditions.

F344 is a strain code used to designate an outbred stock of rats that has been inbreeded for over 100 generations. The F344 rats, also known as Fischer 344 rats, were originally developed at the National Institutes of Health (NIH) and are now widely used in biomedical research due to their consistent and reliable genetic background.

Inbred strains, like the F344, are created by mating genetically identical individuals (siblings or parents and offspring) for many generations until a state of complete homozygosity is reached, meaning that all members of the strain have identical genomes. This genetic uniformity makes inbred strains ideal for use in studies where consistent and reproducible results are important.

F344 rats are known for their longevity, with a median lifespan of around 27-31 months, making them useful for aging research. They also have a relatively low incidence of spontaneous tumors compared to other rat strains. However, they may be more susceptible to certain types of cancer and other diseases due to their inbred status.

It's important to note that while F344 rats are often used as a standard laboratory rat strain, there can still be some genetic variation between individual animals within the same strain, particularly if they come from different suppliers or breeding colonies. Therefore, it's always important to consider the source and history of any animal model when designing experiments and interpreting results.

The brainstem is the lower part of the brain that connects to the spinal cord. It consists of the midbrain, pons, and medulla oblongata. The brainstem controls many vital functions such as heart rate, breathing, and blood pressure. It also serves as a relay center for sensory and motor information between the cerebral cortex and the rest of the body. Additionally, several cranial nerves originate from the brainstem, including those that control eye movements, facial movements, and hearing.

Molecular targeted therapy is a type of treatment that targets specific molecules involved in the growth, progression, and spread of cancer. These molecules can be proteins, genes, or other molecules that contribute to the development of cancer. By targeting these specific molecules, molecular targeted therapy aims to block the abnormal signals that promote cancer growth and progression, thereby inhibiting or slowing down the growth of cancer cells while minimizing harm to normal cells.

Examples of molecular targeted therapies include monoclonal antibodies, tyrosine kinase inhibitors, angiogenesis inhibitors, and immunotherapies that target specific immune checkpoints. These therapies can be used alone or in combination with other cancer treatments such as chemotherapy, radiation therapy, or surgery. The goal of molecular targeted therapy is to improve the effectiveness of cancer treatment while reducing side effects and improving quality of life for patients.

Memantine is an antagonist of the N-methyl-D-aspartate (NMDA) receptor, which is a type of glutamate receptor found in nerve cells. It is primarily used to treat moderate to severe Alzheimer's disease, as it can help slow down cognitive decline and improve symptoms such as memory loss, confusion, and problems with thinking and reasoning. Memantine works by blocking the excessive activation of NMDA receptors, which can contribute to the damage and death of nerve cells in the brain associated with Alzheimer's disease. It is available in oral formulations, including tablets, capsules, and oral solution.

Copper is a chemical element with the symbol Cu (from Latin: *cuprum*) and atomic number 29. It is a soft, malleable, and ductile metal with very high thermal and electrical conductivity. Copper is found as a free element in nature, and it is also a constituent of many minerals such as chalcopyrite and bornite.

In the human body, copper is an essential trace element that plays a role in various physiological processes, including iron metabolism, energy production, antioxidant defense, and connective tissue synthesis. Copper is found in a variety of foods, such as shellfish, nuts, seeds, whole grains, and organ meats. The recommended daily intake of copper for adults is 900 micrograms (mcg) per day.

Copper deficiency can lead to anemia, neutropenia, impaired immune function, and abnormal bone development. Copper toxicity, on the other hand, can cause nausea, vomiting, abdominal pain, diarrhea, and in severe cases, liver damage and neurological symptoms. Therefore, it is important to maintain a balanced copper intake through diet and supplements if necessary.

Ceruloplasmin is a protein found in blood plasma that binds and transports copper ions. It plays a crucial role in copper metabolism, including the oxidation of ferrous iron to ferric iron, which is necessary for the incorporation of iron into transferrin, another protein responsible for transporting iron throughout the body. Ceruloplasmin also acts as an antioxidant by scavenging free radicals and has been implicated in neurodegenerative disorders like Alzheimer's disease and Wilson's disease, a genetic disorder characterized by abnormal copper accumulation in various organs.

The basal ganglia are a group of interconnected nuclei, or clusters of neurons, located in the base of the brain. They play a crucial role in regulating motor function, cognition, and emotion. The main components of the basal ganglia include the striatum (made up of the caudate nucleus, putamen, and ventral striatum), globus pallidus (divided into external and internal segments), subthalamic nucleus, and substantia nigra (with its pars compacta and pars reticulata).

The basal ganglia receive input from various regions of the cerebral cortex and other brain areas. They process this information and send output back to the thalamus and cortex, helping to modulate and coordinate movement. The basal ganglia also contribute to higher cognitive functions such as learning, decision-making, and habit formation. Dysfunction in the basal ganglia can lead to neurological disorders like Parkinson's disease, Huntington's disease, and dystonia.

Embryonic stem cells are a type of pluripotent stem cell that are derived from the inner cell mass of a blastocyst, which is a very early-stage embryo. These cells have the ability to differentiate into any cell type in the body, making them a promising area of research for regenerative medicine and the study of human development and disease. Embryonic stem cells are typically obtained from surplus embryos created during in vitro fertilization (IVF) procedures, with the consent of the donors. The use of embryonic stem cells is a controversial issue due to ethical concerns surrounding the destruction of human embryos.

Fragile X syndrome is a genetic disorder caused by a mutation in the FMR1 gene, which provides instructions for making a protein called fragile X mental retardation protein (FMRP). This protein is essential for normal brain development.

In people with Fragile X syndrome, the FMR1 gene is missing a critical piece of DNA, leading to little or no production of FMRP. As a result, the brain's nerve cells cannot develop and function normally, which can cause a range of developmental problems, including learning disabilities, cognitive impairment, and behavioral and emotional difficulties.

Fragile X syndrome is the most common form of inherited intellectual disability, affecting about 1 in 4,000 males and 1 in 8,000 females. The symptoms and severity can vary widely, but most people with Fragile X syndrome have some degree of intellectual disability, ranging from mild to severe. They may also have physical features associated with the condition, such as a long face, large ears, flexible joints, and flat feet.

There is no cure for Fragile X syndrome, but early intervention and treatment can help improve outcomes. Treatment typically involves a combination of educational support, behavioral therapy, speech and language therapy, physical therapy, and medication to manage symptoms such as anxiety, hyperactivity, and aggression.

Antiparkinson agents are a class of medications used to treat the symptoms of Parkinson's disease and related disorders. These agents work by increasing the levels or activity of dopamine, a neurotransmitter in the brain that is responsible for regulating movement and coordination.

There are several types of antiparkinson agents, including:

1. Levodopa: This is the most effective treatment for Parkinson's disease. It is converted to dopamine in the brain and helps to replace the missing dopamine in people with Parkinson's.
2. Dopamine agonists: These medications mimic the effects of dopamine in the brain and can be used alone or in combination with levodopa. Examples include pramipexole, ropinirole, and rotigotine.
3. Monoamine oxidase B (MAO-B) inhibitors: These medications block the breakdown of dopamine in the brain and can help to increase its levels. Examples include selegiline and rasagiline.
4. Catechol-O-methyltransferase (COMT) inhibitors: These medications block the breakdown of levodopa in the body, allowing it to reach the brain in higher concentrations. Examples include entacapone and tolcapone.
5. Anticholinergic agents: These medications block the action of acetylcholine, another neurotransmitter that can contribute to tremors and muscle stiffness in Parkinson's disease. Examples include trihexyphenidyl and benztropine.

It is important to note that antiparkinson agents can have side effects, and their use should be carefully monitored by a healthcare professional. The choice of medication will depend on the individual patient's symptoms, age, overall health, and other factors.

Autoimmune encephalomyelitis (EAE) is a model of inflammatory demyelinating disease used in medical research to study the mechanisms of multiple sclerosis (MS) and develop new therapies. It is experimentally induced in laboratory animals, typically mice or rats, through immunization with myelin antigens or T-cell transfer. The resulting immune response leads to inflammation, demyelination, and neurological dysfunction in the central nervous system (CNS), mimicking certain aspects of MS.

EAE is a valuable tool for understanding the pathogenesis of MS and testing potential treatments. However, it is essential to recognize that EAE is an experimental model and may not fully recapitulate all features of human autoimmune encephalomyelitis.

Energy metabolism is the process by which living organisms produce and consume energy to maintain life. It involves a series of chemical reactions that convert nutrients from food, such as carbohydrates, fats, and proteins, into energy in the form of adenosine triphosphate (ATP).

The process of energy metabolism can be divided into two main categories: catabolism and anabolism. Catabolism is the breakdown of nutrients to release energy, while anabolism is the synthesis of complex molecules from simpler ones using energy.

There are three main stages of energy metabolism: glycolysis, the citric acid cycle (also known as the Krebs cycle), and oxidative phosphorylation. Glycolysis occurs in the cytoplasm of the cell and involves the breakdown of glucose into pyruvate, producing a small amount of ATP and nicotinamide adenine dinucleotide (NADH). The citric acid cycle takes place in the mitochondria and involves the further breakdown of pyruvate to produce more ATP, NADH, and carbon dioxide. Oxidative phosphorylation is the final stage of energy metabolism and occurs in the inner mitochondrial membrane. It involves the transfer of electrons from NADH and other electron carriers to oxygen, which generates a proton gradient across the membrane. This gradient drives the synthesis of ATP, producing the majority of the cell's energy.

Overall, energy metabolism is a complex and essential process that allows organisms to grow, reproduce, and maintain their bodily functions. Disruptions in energy metabolism can lead to various diseases, including diabetes, obesity, and neurodegenerative disorders.

DNA damage refers to any alteration in the structure or composition of deoxyribonucleic acid (DNA), which is the genetic material present in cells. DNA damage can result from various internal and external factors, including environmental exposures such as ultraviolet radiation, tobacco smoke, and certain chemicals, as well as normal cellular processes such as replication and oxidative metabolism.

Examples of DNA damage include base modifications, base deletions or insertions, single-strand breaks, double-strand breaks, and crosslinks between the two strands of the DNA helix. These types of damage can lead to mutations, genomic instability, and chromosomal aberrations, which can contribute to the development of diseases such as cancer, neurodegenerative disorders, and aging-related conditions.

The body has several mechanisms for repairing DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. However, if the damage is too extensive or the repair mechanisms are impaired, the cell may undergo apoptosis (programmed cell death) to prevent the propagation of potentially harmful mutations.

Transgenic rats are genetically modified rats that have incorporated foreign DNA (transgene) into their own genome. This is typically done through the use of recombinant DNA techniques in the laboratory. The transgene can come from any species, including other mammals, plants, or even bacteria. Once the transgene is introduced into the rat's embryonic cells, it becomes a permanent part of the rat's genetic makeup and is passed on to its offspring.

Transgenic rats are used in biomedical research as models for studying human diseases, developing new therapies, and testing the safety and efficacy of drugs. They offer several advantages over traditional laboratory rats, including the ability to manipulate specific genes, study gene function and regulation, and investigate the underlying mechanisms of disease.

Some common applications of transgenic rats in research include:

1. Modeling human diseases: Transgenic rats can be engineered to develop symptoms and characteristics of human diseases, such as cancer, diabetes, Alzheimer's, and Parkinson's. This allows researchers to study the disease progression, test new treatments, and evaluate their effectiveness.
2. Gene function and regulation: By introducing specific genes into rats, scientists can investigate their role in various biological processes, such as development, aging, and metabolism. They can also study how genes are regulated and how they interact with each other.
3. Drug development and testing: Transgenic rats can be used to test the safety and efficacy of new drugs before they are tested in humans. By studying the effects of drugs on transgenic rats, researchers can gain insights into their potential benefits and risks.
4. Toxicology studies: Transgenic rats can be used to study the toxicity of chemicals, pollutants, and other substances. This helps ensure that new products and treatments are safe for human use.

In summary, transgenic rats are genetically modified rats that have incorporated foreign DNA into their own genome. They are widely used in biomedical research to model human diseases, study gene function and regulation, develop new therapies, and test the safety and efficacy of drugs.

Neurofibrils are thin, thread-like structures found within the cytoplasm of nerve cells (neurons). They are primarily composed of various proteins and are involved in maintaining the structure and function of neurons. Neurofibrils include two types: neurofilaments and microtubule-associated protein tau (TAU) proteins.

Neurofilaments are intermediate filaments that provide structural support to neurons, while TAU proteins are involved in microtubule assembly, stability, and intracellular transport. Abnormal accumulation and aggregation of these proteins can lead to neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS).

Coculture techniques refer to a type of experimental setup in which two or more different types of cells or organisms are grown and studied together in a shared culture medium. This method allows researchers to examine the interactions between different cell types or species under controlled conditions, and to study how these interactions may influence various biological processes such as growth, gene expression, metabolism, and signal transduction.

Coculture techniques can be used to investigate a wide range of biological phenomena, including the effects of host-microbe interactions on human health and disease, the impact of different cell types on tissue development and homeostasis, and the role of microbial communities in shaping ecosystems. These techniques can also be used to test the efficacy and safety of new drugs or therapies by examining their effects on cells grown in coculture with other relevant cell types.

There are several different ways to establish cocultures, depending on the specific research question and experimental goals. Some common methods include:

1. Mixed cultures: In this approach, two or more cell types are simply mixed together in a culture dish or flask and allowed to grow and interact freely.
2. Cell-layer cultures: Here, one cell type is grown on a porous membrane or other support structure, while the second cell type is grown on top of it, forming a layered coculture.
3. Conditioned media cultures: In this case, one cell type is grown to confluence and its culture medium is collected and then used to grow a second cell type. This allows the second cell type to be exposed to any factors secreted by the first cell type into the medium.
4. Microfluidic cocultures: These involve growing cells in microfabricated channels or chambers, which allow for precise control over the spatial arrangement and flow of nutrients, waste products, and signaling molecules between different cell types.

Overall, coculture techniques provide a powerful tool for studying complex biological systems and gaining insights into the mechanisms that underlie various physiological and pathological processes.

Gene knockdown techniques are methods used to reduce the expression or function of specific genes in order to study their role in biological processes. These techniques typically involve the use of small RNA molecules, such as siRNAs (small interfering RNAs) or shRNAs (short hairpin RNAs), which bind to and promote the degradation of complementary mRNA transcripts. This results in a decrease in the production of the protein encoded by the targeted gene.

Gene knockdown techniques are often used as an alternative to traditional gene knockout methods, which involve completely removing or disrupting the function of a gene. Knockdown techniques allow for more subtle and reversible manipulation of gene expression, making them useful for studying genes that are essential for cell survival or have redundant functions.

These techniques are widely used in molecular biology research to investigate gene function, genetic interactions, and disease mechanisms. However, it is important to note that gene knockdown can have off-target effects and may not completely eliminate the expression of the targeted gene, so results should be interpreted with caution.

Reactive Nitrogen Species (RNS) are a group of highly reactive and chemically diverse molecules that are derived from nitric oxide (NO) or other nitrogen-containing compounds. They play important roles in various biological processes, such as cell signaling, neurotransmission, and immune response. However, an overproduction of RNS can also contribute to the development of several pathological conditions, including inflammation, neurodegenerative diseases, and cancer. Examples of RNS include nitric oxide (NO), peroxynitrite (ONOO-), and nitrogen dioxide (NO2). These species are generated through various biochemical reactions, such as the conversion of L-arginine to citrulline by nitric oxide synthase (NOS) enzymes, which leads to the production of NO. RNS can then react with other molecules in the body, such as reactive oxygen species (ROS), leading to the formation of harmful compounds that can damage cellular structures and disrupt normal physiological functions.

Intermediate filament proteins (IFPs) are a type of cytoskeletal protein that form the intermediate filaments (IFs), which are one of the three major components of the cytoskeleton in eukaryotic cells, along with microtubules and microfilaments. These proteins have a unique structure, characterized by an alpha-helical rod domain flanked by non-helical head and tail domains.

Intermediate filament proteins are classified into six major types based on their amino acid sequence: Type I (acidic) and Type II (basic) keratins, Type III (desmin, vimentin, glial fibrillary acidic protein, and peripherin), Type IV (neurofilaments), Type V (lamins), and Type VI (nestin). Each type of IFP has a distinct pattern of expression in different tissues and cell types.

Intermediate filament proteins play important roles in maintaining the structural integrity and mechanical strength of cells, providing resilience to mechanical stress, and regulating various cellular processes such as cell division, migration, and signal transduction. Mutations in IFP genes have been associated with several human diseases, including cancer, neurodegenerative disorders, and genetic skin fragility disorders.

Stilbenes are a type of chemical compound that consists of a 1,2-diphenylethylene backbone. They are phenolic compounds and can be found in various plants, where they play a role in the defense against pathogens and stress conditions. Some stilbenes have been studied for their potential health benefits, including their antioxidant and anti-inflammatory effects. One well-known example of a stilbene is resveratrol, which is found in the skin of grapes and in red wine.

It's important to note that while some stilbenes have been shown to have potential health benefits in laboratory studies, more research is needed to determine their safety and effectiveness in humans. It's always a good idea to talk to a healthcare provider before starting any new supplement regimen.

Bovine spongiform encephalopathy (BSE), also known as "mad cow disease," is a progressive neurodegenerative disorder that affects cattle. It is caused by prions, which are misfolded proteins that can cause other proteins in the brain to also misfold and accumulate, leading to brain damage and degeneration. The disease is named for the sponge-like appearance of the brain tissue that results from this degenerative process.

BSE is a zoonotic disease, which means that it can be transmitted from animals to humans. In humans, BSE is known as variant Creutzfeldt-Jakob disease (vCJD) and is caused by consuming contaminated beef products. The symptoms of vCJD include rapidly progressing dementia, neurological symptoms such as muscle spasms and difficulty coordinating movements, and physical deterioration leading to death.

It's important to note that the use of certain growth promoters in cattle feed and the practice of feeding cattle meat and bone meal have been banned in many countries in order to prevent the spread of BSE. Additionally, strict controls on the inspection and testing of beef products have been implemented to ensure their safety.

Luminescent proteins are a type of protein that emit light through a chemical reaction, rather than by absorbing and re-emitting light like fluorescent proteins. This process is called bioluminescence. The light emitted by luminescent proteins is often used in scientific research as a way to visualize and track biological processes within cells and organisms.

One of the most well-known luminescent proteins is Green Fluorescent Protein (GFP), which was originally isolated from jellyfish. However, GFP is actually a fluorescent protein, not a luminescent one. A true example of a luminescent protein is the enzyme luciferase, which is found in fireflies and other bioluminescent organisms. When luciferase reacts with its substrate, luciferin, it produces light through a process called oxidation.

Luminescent proteins have many applications in research, including as reporters for gene expression, as markers for protein-protein interactions, and as tools for studying the dynamics of cellular processes. They are also used in medical imaging and diagnostics, as well as in the development of new therapies.

Cell culture is a technique used in scientific research to grow and maintain cells from plants, animals, or humans in a controlled environment outside of their original organism. This environment typically consists of a sterile container called a cell culture flask or plate, and a nutrient-rich liquid medium that provides the necessary components for the cells' growth and survival, such as amino acids, vitamins, minerals, and hormones.

There are several different types of cell culture techniques used in research, including:

1. Adherent cell culture: In this technique, cells are grown on a flat surface, such as the bottom of a tissue culture dish or flask. The cells attach to the surface and spread out, forming a monolayer that can be observed and manipulated under a microscope.
2. Suspension cell culture: In suspension culture, cells are grown in liquid medium without any attachment to a solid surface. These cells remain suspended in the medium and can be agitated or mixed to ensure even distribution of nutrients.
3. Organoid culture: Organoids are three-dimensional structures that resemble miniature organs and are grown from stem cells or other progenitor cells. They can be used to study organ development, disease processes, and drug responses.
4. Co-culture: In co-culture, two or more different types of cells are grown together in the same culture dish or flask. This technique is used to study cell-cell interactions and communication.
5. Conditioned medium culture: In this technique, cells are grown in a medium that has been conditioned by previous cultures of other cells. The conditioned medium contains factors secreted by the previous cells that can influence the growth and behavior of the new cells.

Cell culture techniques are widely used in biomedical research to study cellular processes, develop drugs, test toxicity, and investigate disease mechanisms. However, it is important to note that cell cultures may not always accurately represent the behavior of cells in a living organism, and results from cell culture experiments should be validated using other methods.

Proteasome inhibitors are a class of medications that work by blocking the action of proteasomes, which are protein complexes that play a critical role in the breakdown and recycling of damaged or unwanted proteins within cells. By inhibiting the activity of these proteasomes, proteasome inhibitors can cause an accumulation of abnormal proteins within cells, leading to cell death.

This effect is particularly useful in the treatment of certain types of cancer, such as multiple myeloma and mantle cell lymphoma, where malignant cells often have an overproduction of abnormal proteins that can be targeted by proteasome inhibitors. The three main proteasome inhibitors currently approved for use in cancer therapy are bortezomib (Velcade), carfilzomib (Kyprolis), and ixazomib (Ninlaro). These medications have been shown to improve outcomes and extend survival in patients with these types of cancers.

It's important to note that proteasome inhibitors can also have off-target effects on other cells in the body, leading to side effects such as neurotoxicity, gastrointestinal symptoms, and hematologic toxicities. Therefore, careful monitoring and management of these side effects is necessary during treatment with proteasome inhibitors.

Acrolein is an unsaturated aldehyde with the chemical formula CH2CHCHO. It is a colorless liquid that has a distinct unpleasant odor and is highly reactive. Acrolein is produced by the partial oxidation of certain organic compounds, such as glycerol and fatty acids, and it is also found in small amounts in some foods, such as coffee and bread.

Acrolein is a potent irritant to the eyes, nose, and throat, and exposure to high levels can cause coughing, wheezing, and shortness of breath. It has been shown to have toxic effects on the lungs, heart, and nervous system, and prolonged exposure has been linked to an increased risk of cancer.

In the medical field, acrolein is sometimes used as a laboratory reagent or as a preservative for biological specimens. However, due to its potential health hazards, it must be handled with care and appropriate safety precautions should be taken when working with this compound.

An Enzyme-Linked Immunosorbent Assay (ELISA) is a type of analytical biochemistry assay used to detect and quantify the presence of a substance, typically a protein or peptide, in a liquid sample. It takes its name from the enzyme-linked antibodies used in the assay.

In an ELISA, the sample is added to a well containing a surface that has been treated to capture the target substance. If the target substance is present in the sample, it will bind to the surface. Next, an enzyme-linked antibody specific to the target substance is added. This antibody will bind to the captured target substance if it is present. After washing away any unbound material, a substrate for the enzyme is added. If the enzyme is present due to its linkage to the antibody, it will catalyze a reaction that produces a detectable signal, such as a color change or fluorescence. The intensity of this signal is proportional to the amount of target substance present in the sample, allowing for quantification.

ELISAs are widely used in research and clinical settings to detect and measure various substances, including hormones, viruses, and bacteria. They offer high sensitivity, specificity, and reproducibility, making them a reliable choice for many applications.

Tubulin is a type of protein that forms microtubules, which are hollow cylindrical structures involved in the cell's cytoskeleton. These structures play important roles in various cellular processes, including maintaining cell shape, cell division, and intracellular transport. There are two main types of tubulin proteins: alpha-tubulin and beta-tubulin. They polymerize to form heterodimers, which then assemble into microtubules. The assembly and disassembly of microtubules are dynamic processes that are regulated by various factors, including GTP hydrolysis, motor proteins, and microtubule-associated proteins (MAPs). Tubulin is an essential component of the eukaryotic cell and has been a target for anti-cancer drugs such as taxanes and vinca alkaloids.

Lysosomal storage diseases (LSDs) are a group of rare inherited metabolic disorders caused by defects in lysosomal function. These diseases affect many different organ systems, including the nervous system. Lysosomes are membrane-bound organelles found inside cells that break down and recycle various types of cellular waste materials through the action of enzymes. In LSDs, a genetic mutation leads to a deficiency or complete lack of a specific lysosomal enzyme, resulting in the accumulation of undigested substrates within the lysosomes. This accumulation can cause progressive damage to cells and tissues throughout the body, including those in the nervous system.

There are more than 50 different types of LSDs, some of which primarily affect the nervous system:

1. Tay-Sachs disease: A severe neurological disorder caused by a deficiency of the enzyme hexosaminidase A (HEXA). The accumulation of ganglioside GM2 in neurons leads to progressive neurodegeneration, resulting in motor and cognitive decline, blindness, and early death.
2. Sandhoff disease: Similar to Tay-Sachs disease but caused by a deficiency in both HEXA and hexosaminidase B (HEXB) enzymes. This disorder affects multiple organ systems, including the nervous system, with symptoms similar to Tay-Sachs disease but often more severe and rapid progression.
3. GM1 gangliosidosis: A condition caused by a deficiency of the enzyme β-galactosidase (GLB1), leading to the accumulation of GM1 ganglioside in neurons. Symptoms include developmental delay, motor and cognitive decline, seizures, and progressive neurological deterioration.
4. Gaucher disease: A disorder caused by a deficiency of the enzyme glucocerebrosidase (GBA), resulting in the accumulation of glucocerebroside in various tissues, including the nervous system. There are three main types of Gaucher disease, with type 2 and 3 having neurological involvement.
5. Niemann-Pick disease types A and B: These disorders are caused by a deficiency of the enzyme acid sphingomyelinase (SMPD1), leading to the accumulation of sphingomyelin in various tissues, including the nervous system. Type A primarily affects the nervous system, while type B mainly involves visceral organs.
6. Fabry disease: An X-linked disorder caused by a deficiency of the enzyme α-galactosidase A (GLA), resulting in the accumulation of globotriaosylceramide (Gb3) in various tissues, including the nervous system. Symptoms include pain, gastrointestinal issues, skin lesions, and progressive renal, cardiac, and cerebrovascular complications.
7. Metachromatic leukodystrophy: A disorder caused by a deficiency of the enzyme arylsulfatase A (ARSA), leading to the accumulation of sulfatides in the white matter of the brain. Symptoms include motor and cognitive decline, seizures, and progressive neurological deterioration.
8. Krabbe disease: An autosomal recessive disorder caused by a deficiency of the enzyme galactocerebrosidase (GALC), resulting in the accumulation of psychosine in the nervous system. Symptoms include motor and cognitive decline, seizures, and progressive neurological deterioration.
9. Mucopolysaccharidoses: A group of disorders caused by deficiencies of various enzymes involved in the breakdown of glycosaminoglycans (GAGs), leading to their accumulation in tissues throughout the body, including the nervous system. Symptoms vary depending on the specific disorder and include skeletal abnormalities, cardiac complications, vision and hearing loss, and progressive neurological decline.
10. Neuronal ceroid lipofuscinoses: A group of neurodegenerative disorders caused by mutations in various genes involved in lysosomal function, leading to the accumulation of lipopigments in neurons and other cells. Symptoms include seizures, motor and cognitive decline, vision loss, and progressive neurological deterioration.
11. Peroxisomal biogenesis disorders: A group of disorders caused by mutations in genes involved in peroxisome biogenesis, leading to the accumulation of very long-chain fatty acids, phytanic acid, and pipecolic acid in tissues throughout the body, including the nervous system. Symptoms vary depending on the specific disorder and include developmental delay, hypotonia, seizures, vision loss, hearing impairment, and progressive neurological decline.
12. Congenital disorders of glycosylation: A group of disorders caused by mutations in genes involved in N-glycosylation, leading to abnormal protein folding, trafficking, and function. Symptoms vary depending on the specific disorder and include developmental delay, hypotonia, seizures, vision loss, hearing impairment, and progressive neurological decline.
13. Leukodystrophies: A group of disorders characterized by abnormalities in the white matter of the brain due to defects in myelin formation or maintenance. Symptoms vary depending on the specific disorder and include developmental delay, hypotonia, seizures, vision loss, hearing impairment, and progressive neurological decline.
14. Mitochondrial disorders: A group of disorders caused by mutations in genes involved in mitochondrial function, leading to energy production deficits and oxidative stress. Symptoms vary depending on the specific disorder and include developmental delay, hypotonia, seizures, vision loss, hearing impairment, and progressive neurological decline.
15. Neurodegenerative disorders: A group of disorders characterized by progressive degeneration of the nervous system, leading to cognitive decline, motor dysfunction, and ultimately death. Examples include Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis (ALS).
16. Neurodevelopmental disorders: A group of disorders characterized by impairments in cognitive, social, and motor development, including autism spectrum disorder, attention deficit hyperactivity disorder (ADHD), intellectual disability, and specific learning disorders.
17. Epilepsy: A group of disorders characterized by recurrent seizures due to abnormal electrical activity in the brain. Epilepsy can be caused by various genetic and environmental factors, including structural brain abnormalities, infections, trauma, and metabolic imbalances.
18. Neuroinflammatory disorders: A group of disorders characterized by inflammation of the nervous system, leading to damage and dysfunction. Examples include multiple sclerosis, neuromyelitis optica, and autoimmune encephalitis.
19. Infectious diseases of the nervous system: A group of disorders caused by infectious agents such as viruses, bacteria, fungi, or parasites that affect the nervous system. Examples include meningitis, encephalitis, and HIV-associated neurological disorders.
20. Neurotoxic disorders: A group of disorders caused by exposure to neurotoxic substances such as heavy metals, pesticides, solvents, or drugs that damage the nervous system. Examples include lead poisoning, organophosphate poisoning, and methanol toxicity.
21. Neurooncological disorders: A group of disorders characterized by tumors of the nervous system, including primary brain tumors, metastatic brain tumors, and spinal cord tumors.
22. Vascular disorders of the nervous system: A group of disorders caused by disruption of blood flow to the nervous system, leading to ischemia or hemorrhage. Examples include stroke, transient ischemic attack, and subarachnoid hemorrhage.
23. Degenerative disorders of the nervous system: A group of disorders characterized by progressive degeneration of nerve cells and their supporting structures, leading to functional impairment. Examples include Alzheimer's disease, Parkinson's disease, and Huntington's disease.
24. Neurodevelopmental disorders: A group of disorders that affect the development of the nervous system, leading to cognitive, behavioral, or motor impairments. Examples include autism spectrum disorder, attention deficit hyperactivity disorder, and intellectual disability.
25. Epilepsy and seizure disorders: A group of disorders characterized by recurrent seizures, which are abnormal electrical discharges in the brain that can cause a variety of symptoms such as convulsions, altered consciousness, or sensory disturbances.
26. Neurogenetic disorders: A group of disorders caused by genetic mutations that affect the structure or function of the nervous system. Examples include fragile X syndrome, tuberous sclerosis complex, and neurofibromatosis type 1.
27. Neuromuscular

Mild Cognitive Impairment (MCI) is a medical term used to describe a stage between the cognitive changes seen in normal aging and the more serious decline of dementia. It's characterized by a slight but noticeable decline in cognitive abilities, such as memory or thinking skills, that are greater than expected for an individual's age and education level, but not significant enough to interfere with daily life.

People with MCI have an increased risk of developing dementia, particularly Alzheimer's disease, compared to those without MCI. However, it's important to note that not everyone with MCI will develop dementia; some may remain stable, and others may even improve over time.

The diagnosis of MCI is typically made through a comprehensive medical evaluation, including a detailed medical history, cognitive testing, and sometimes brain imaging or laboratory tests.

Alternative splicing is a process in molecular biology that occurs during the post-transcriptional modification of pre-messenger RNA (pre-mRNA) molecules. It involves the removal of non-coding sequences, known as introns, and the joining together of coding sequences, or exons, to form a mature messenger RNA (mRNA) molecule that can be translated into a protein.

In alternative splicing, different combinations of exons are selected and joined together to create multiple distinct mRNA transcripts from a single pre-mRNA template. This process increases the diversity of proteins that can be produced from a limited number of genes, allowing for greater functional complexity in organisms.

Alternative splicing is regulated by various cis-acting elements and trans-acting factors that bind to specific sequences in the pre-mRNA molecule and influence which exons are included or excluded during splicing. Abnormal alternative splicing has been implicated in several human diseases, including cancer, neurological disorders, and cardiovascular disease.

A "mutant strain of mice" in a medical context refers to genetically engineered mice that have specific genetic mutations introduced into their DNA. These mutations can be designed to mimic certain human diseases or conditions, allowing researchers to study the underlying biological mechanisms and test potential therapies in a controlled laboratory setting.

Mutant strains of mice are created through various techniques, including embryonic stem cell manipulation, gene editing technologies such as CRISPR-Cas9, and radiation-induced mutagenesis. These methods allow scientists to introduce specific genetic changes into the mouse genome, resulting in mice that exhibit altered physiological or behavioral traits.

These strains of mice are widely used in biomedical research because their short lifespan, small size, and high reproductive rate make them an ideal model organism for studying human diseases. Additionally, the mouse genome has been well-characterized, and many genetic tools and resources are available to researchers working with these animals.

Examples of mutant strains of mice include those that carry mutations in genes associated with cancer, neurodegenerative disorders, metabolic diseases, and immunological conditions. These mice provide valuable insights into the pathophysiology of human diseases and help advance our understanding of potential therapeutic interventions.

Intermediate filaments (IFs) are a type of cytoskeletal filament found in the cytoplasm of eukaryotic cells, including animal cells. They are called "intermediate" because they are smaller in diameter than microfilaments and larger than microtubules, two other types of cytoskeletal structures.

Intermediate filaments are composed of fibrous proteins that form long, unbranched, and flexible filaments. These filaments provide structural support to the cell and help maintain its shape. They also play a role in cell-to-cell adhesion, intracellular transport, and protection against mechanical stress.

Intermediate filaments are classified into six types based on their protein composition: Type I (acidic keratins), Type II (neutral/basic keratins), Type III (vimentin, desmin, peripherin), Type IV (neurofilaments), Type V (lamins), and Type VI (nestin). Each type of intermediate filament has a specific function and is expressed in different cell types. For example, Type I and II keratins are found in epithelial cells, while vimentin is expressed in mesenchymal cells.

Overall, intermediate filaments play an essential role in maintaining the structural integrity of cells and tissues, and their dysfunction has been implicated in various human diseases, including cancer, neurodegenerative disorders, and genetic disorders.

Amino acid repetitive sequences refer to patterns of amino acids that are repeated in a polypeptide chain. These repetitions can vary in length and can be composed of a single type of amino acid or a combination of different types. In some cases, expansions of these repetitive sequences can lead to the production of abnormal proteins that are associated with certain genetic disorders. The expansion of trinucleotide repeats that code for particular amino acids is one example of this phenomenon. These expansions can result in protein misfolding and aggregation, leading to neurodegenerative diseases such as Huntington's disease and spinocerebellar ataxias.

Kynurenine 3-Monooxygenase (KMO) is an enzyme that is involved in the metabolism of the amino acid tryptophan. Specifically, it is a key enzyme in the kynurenine pathway, which is the primary route of tryptophan breakdown in mammals.

KMO catalyzes the conversion of L-kynurenine to 3-hydroxykynurenine using molecular oxygen and nicotinamide adenine dinucleotide phosphate (NADPH) as cofactors. This reaction is an important step in the production of several neuroactive metabolites, including quinolinic acid and kynurenic acid, which have been implicated in various neurological disorders such as Alzheimer's disease, Parkinson's disease, and depression.

Inhibition of KMO has been suggested as a potential therapeutic strategy for the treatment of these disorders due to its role in regulating the balance between neuroprotective and neurotoxic kynurenine metabolites.

Neurological models are simplified representations or simulations of various aspects of the nervous system, including its structure, function, and processes. These models can be theoretical, computational, or physical and are used to understand, explain, and predict neurological phenomena. They may focus on specific neurological diseases, disorders, or functions, such as memory, learning, or movement. The goal of these models is to provide insights into the complex workings of the nervous system that cannot be easily observed or understood through direct examination alone.

Dendrites are the branched projections of a neuron that receive and process signals from other neurons. They are typically short and highly branching, increasing the surface area for receiving incoming signals. Dendrites are covered in small protrusions called dendritic spines, which can form connections with the axon terminals of other neurons through chemical synapses. The structure and function of dendrites play a critical role in the integration and processing of information in the nervous system.

Ubiquinone, also known as coenzyme Q10 (CoQ10), is a lipid-soluble benzoquinone that plays a crucial role in the mitochondrial electron transport chain as an essential component of Complexes I, II, and III. It functions as an electron carrier, assisting in the transfer of electrons from reduced nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH2) to molecular oxygen during oxidative phosphorylation, thereby contributing to the generation of adenosine triphosphate (ATP), the primary energy currency of the cell.

Additionally, ubiquinone acts as a potent antioxidant in both membranes and lipoproteins, protecting against lipid peroxidation and oxidative damage to proteins and DNA. Its antioxidant properties stem from its ability to donate electrons and regenerate other antioxidants like vitamin E. Ubiquinone is synthesized endogenously in all human cells, with the highest concentrations found in tissues with high energy demands, such as the heart, liver, kidneys, and skeletal muscles.

Deficiency in ubiquinone can result from genetic disorders, aging, or certain medications (such as statins), leading to impaired mitochondrial function and increased oxidative stress. Supplementation with ubiquinone has been explored as a potential therapeutic strategy for various conditions associated with mitochondrial dysfunction and oxidative stress, including cardiovascular diseases, neurodegenerative disorders, and cancer.

Antioxidant Response Elements (AREs) are specific sequences of DNA that bind to transcription factors and regulate the expression of genes involved in the antioxidant response. These elements are typically found in the promoter region of genes that encode for proteins involved in protecting cells against oxidative stress, such as enzymes that detoxify reactive oxygen species (ROS) or repair damaged cellular components.

The most well-known transcription factor that binds to AREs is Nrf2 (nuclear factor erythroid 2-related factor 2). Under normal conditions, Nrf2 is bound to its inhibitor protein Keap1 in the cytoplasm and is targeted for degradation. However, under oxidative stress conditions, ROS or other electrophilic molecules can modify Keap1, leading to the release and activation of Nrf2. Activated Nrf2 then translocates to the nucleus and binds to AREs, inducing the expression of antioxidant response genes.

Therefore, AREs play a critical role in regulating the cellular response to oxidative stress and protecting cells from damage caused by ROS and other harmful molecules.

A lentivirus is a type of slow-acting retrovirus that can cause chronic diseases and cancers. The term "lentivirus" comes from the Latin word "lentus," which means slow. Lentiviruses are characterized by their ability to establish a persistent infection, during which they continuously produce new viral particles.

Lentiviruses have a complex genome that includes several accessory genes, in addition to the typical gag, pol, and env genes found in all retroviruses. These accessory genes play important roles in regulating the virus's replication cycle and evading the host's immune response.

One of the most well-known lentiviruses is the human immunodeficiency virus (HIV), which causes AIDS. Other examples include the feline immunodeficiency virus (FIV) and the simian immunodeficiency virus (SIV). Lentiviruses have also been used as vectors for gene therapy, as they can efficiently introduce new genes into both dividing and non-dividing cells.

A genetic vector is a vehicle, often a plasmid or a virus, that is used to introduce foreign DNA into a host cell as part of genetic engineering or gene therapy techniques. The vector contains the desired gene or genes, along with regulatory elements such as promoters and enhancers, which are needed for the expression of the gene in the target cells.

The choice of vector depends on several factors, including the size of the DNA to be inserted, the type of cell to be targeted, and the efficiency of uptake and expression required. Commonly used vectors include plasmids, adenoviruses, retroviruses, and lentiviruses.

Plasmids are small circular DNA molecules that can replicate independently in bacteria. They are often used as cloning vectors to amplify and manipulate DNA fragments. Adenoviruses are double-stranded DNA viruses that infect a wide range of host cells, including human cells. They are commonly used as gene therapy vectors because they can efficiently transfer genes into both dividing and non-dividing cells.

Retroviruses and lentiviruses are RNA viruses that integrate their genetic material into the host cell's genome. This allows for stable expression of the transgene over time. Lentiviruses, a subclass of retroviruses, have the advantage of being able to infect non-dividing cells, making them useful for gene therapy applications in post-mitotic tissues such as neurons and muscle cells.

Overall, genetic vectors play a crucial role in modern molecular biology and medicine, enabling researchers to study gene function, develop new therapies, and modify organisms for various purposes.

Beta-N-Acetylhexosaminidases are a group of enzymes that play a role in the breakdown and recycling of complex carbohydrates in the body. Specifically, they help to break down gangliosides, which are a type of molecule found in cell membranes.

There are several different isoforms of beta-N-Acetylhexosaminidases, including A, B, and S. These isoforms are formed by different combinations of subunits, which can affect their activity and substrate specificity.

Mutations in the genes that encode for these enzymes can lead to a variety of genetic disorders, including Tay-Sachs disease and Sandhoff disease. These conditions are characterized by an accumulation of gangliosides in the brain, which can cause progressive neurological deterioration and death.

Treatment for these conditions typically involves managing symptoms and providing supportive care, as there is currently no cure. Enzyme replacement therapy has been explored as a potential treatment option, but its effectiveness varies depending on the specific disorder and the age of the patient.

Electron Transport Complex I, also known as NADH:ubiquinone oxidoreductase, is a large protein complex located in the inner mitochondrial membrane of eukaryotic cells and the cytoplasmic membrane of prokaryotic cells. It is the first complex in the electron transport chain, a series of protein complexes that transfer electrons from NADH to oxygen, driving the synthesis of ATP through chemiosmosis.

Complex I consists of multiple subunits, including a flavin mononucleotide (FMN) cofactor and several iron-sulfur clusters, which facilitate the oxidation of NADH and the reduction of ubiquinone (coenzyme Q). The energy released during this electron transfer process is used to pump protons across the membrane, creating a proton gradient that drives ATP synthesis.

Defects in Complex I can lead to various mitochondrial diseases, including neurological disorders and muscle weakness.

Mucopolysaccharidosis III, also known as Sanfilippo syndrome, is a genetic disorder caused by the deficiency of specific enzymes needed to break down complex sugar molecules called glycosaminoglycans (GAGs) or mucopolysaccharides. This results in an accumulation of these substances in various tissues and organs, leading to progressive damage.

There are four main types of Mucopolysaccharidosis III (A, B, C, and D), each caused by a deficiency in one of the following enzymes: heparan N-sulfatase (type A), alpha-N-acetylglucosaminidase (type B), acetyl-CoAlpha-glucosaminide acetyltransferase (type C), or N-acetylglucosamine 6-sulfatase (type D).

The symptoms of Mucopolysaccharidosis III typically become apparent between the ages of 2 and 6, and may include developmental delays, hyperactivity, behavioral problems, sleep disturbances, coarse facial features, hirsutism, hepatosplenomegaly (enlarged liver and spleen), and joint stiffness. Over time, individuals with Mucopolysaccharidosis III may experience a decline in cognitive abilities, loss of previously acquired skills, and mobility issues.

Currently, there is no cure for Mucopolysaccharidosis III, and treatment is focused on managing the symptoms and improving quality of life. Enzyme replacement therapy, gene therapy, and stem cell transplantation are some of the experimental treatments being investigated for this condition.

Tissue distribution, in the context of pharmacology and toxicology, refers to the way that a drug or xenobiotic (a chemical substance found within an organism that is not naturally produced by or expected to be present within that organism) is distributed throughout the body's tissues after administration. It describes how much of the drug or xenobiotic can be found in various tissues and organs, and is influenced by factors such as blood flow, lipid solubility, protein binding, and the permeability of cell membranes. Understanding tissue distribution is important for predicting the potential effects of a drug or toxin on different parts of the body, and for designing drugs with improved safety and efficacy profiles.

The Fluorescent Antibody Technique (FAT) is a type of immunofluorescence assay used in laboratory medicine and pathology for the detection and localization of specific antigens or antibodies in tissues, cells, or microorganisms. In this technique, a fluorescein-labeled antibody is used to selectively bind to the target antigen or antibody, forming an immune complex. When excited by light of a specific wavelength, the fluorescein label emits light at a longer wavelength, typically visualized as green fluorescence under a fluorescence microscope.

The FAT is widely used in diagnostic microbiology for the identification and characterization of various bacteria, viruses, fungi, and parasites. It has also been applied in the diagnosis of autoimmune diseases and certain cancers by detecting specific antibodies or antigens in patient samples. The main advantage of FAT is its high sensitivity and specificity, allowing for accurate detection and differentiation of various pathogens and disease markers. However, it requires specialized equipment and trained personnel to perform and interpret the results.

Endoplasmic reticulum-associated degradation (ERAD) is a cellular process that targets and degrades misfolded or damaged proteins located in the endoplasmic reticulum (ER). The ER is a network of membrane-bound tubules and sacs within eukaryotic cells where proteins are synthesized, folded, and modified before being transported to their final destinations.

When proteins fail to fold correctly or become damaged in the ER, they can be recognized and tagged for degradation through the ERAD pathway. This process involves several steps:

1. Recognition: Misfolded or damaged proteins are recognized by specific chaperone proteins and ubiquitin ligases in the ER. Chaperones help proteins fold correctly, while ubiquitin ligases tag misfolded proteins with ubiquitin molecules, marking them for degradation.
2. Retrotranslocation: The marked proteins are then retrotranslocated (or "pulled back") across the ER membrane into the cytosol by a protein complex called the ERAD machinery.
3. Ubiquitination: Once in the cytosol, the ubiquitin molecules attached to the misfolded proteins are recognized by another set of ubiquitin ligases, which add more ubiquitin molecules, creating a polyubiquitin chain.
4. Degradation: The polyubiquitinated protein is then targeted to and degraded by the 26S proteasome, a large protein complex responsible for breaking down unwanted or damaged proteins in the cell.

ERAD plays a crucial role in maintaining protein quality control and ensuring proper cellular function. Dysregulation of ERAD has been implicated in various diseases, including neurodegenerative disorders, cancer, and viral infections.

I'm sorry for any confusion, but "mitochondrial turnover" is not a widely recognized or established medical term with a specific definition. Mitochondria are the powerhouses of the cell, responsible for producing energy in the form of ATP through a process called oxidative phosphorylation.

The term "turnover," when used in a biological context, generally refers to the process by which cells replace or regenerate their components over time. Therefore, one might infer that "mitochondrial turnover" could refer to the replacement and regeneration of mitochondria within cells. However, this is not a standardized term, and its precise meaning could vary depending on the context.

Mitochondria are known to undergo dynamic processes such as fusion (combining) and fission (dividing), which allow them to change their size, shape, and distribution in response to cellular needs. Additionally, damaged or dysfunctional mitochondria can be removed through a process called mitophagy, where they're targeted for degradation within lysosomes. New, healthy mitochondria are generated through biogenesis, which involves the production of new mitochondrial proteins and membranes.

In summary, while "mitochondrial turnover" is not a standard medical term, it could be used to describe the ongoing processes of mitochondrial dynamics, mitophagy, and biogenesis that contribute to the replacement and regeneration of mitochondria within cells over time.

Cell respiration is the process by which cells convert biochemical energy from nutrients into adenosine triphosphate (ATP), and then release waste products. The three main stages of cell respiration are glycolysis, the citric acid cycle (also known as the Krebs cycle), and the electron transport chain.

During glycolysis, which takes place in the cytoplasm, glucose is broken down into two molecules of pyruvate, producing a small amount of ATP and reducing power in the form of NADH.

The citric acid cycle occurs in the mitochondria and involves the breakdown of acetyl-CoA (formed from pyruvate) to produce more ATP, NADH, and FADH2.

Finally, the electron transport chain, also located in the mitochondria, uses the energy from NADH and FADH2 to pump protons across the inner mitochondrial membrane, creating a proton gradient. The flow of protons back across the membrane drives the synthesis of ATP, which is used as a source of energy by the cell.

Cell respiration is a crucial process that allows cells to generate the energy they need to perform various functions and maintain homeostasis.

Acetylcysteine is a medication that is used for its antioxidant effects and to help loosen thick mucus in the lungs. It is commonly used to treat conditions such as chronic bronchitis, emphysema, and cystic fibrosis. Acetylcysteine is also known by the brand names Mucomyst and Accolate. It works by thinning and breaking down mucus in the airways, making it easier to cough up and clear the airways. Additionally, acetylcysteine is an antioxidant that helps to protect cells from damage caused by free radicals. It is available as a oral tablet, liquid, or inhaled medication.

The S100 calcium binding protein beta subunit, also known as S100B, is a member of the S100 family of proteins. These proteins are characterized by their ability to bind calcium ions and play a role in intracellular signaling pathways. The S100B protein is made up of two subunits, alpha and beta, which form a homodimer. It is primarily expressed in astrocytes, a type of glial cell found in the central nervous system.

S100B has been shown to have both intracellular and extracellular functions. Inside cells, it regulates various processes such as the dynamics of cytoskeleton, calcium homeostasis and cell proliferation. Extracellularly, S100B acts as a damage-associated molecular pattern (DAMP) molecule, released from damaged or stressed cells, where it can interact with receptors on other cells to induce inflammatory responses, neuronal death and contribute to the pathogenesis of several neurological disorders.

Elevated levels of S100B in cerebrospinal fluid (CSF) or blood are associated with various central nervous system injuries such as traumatic brain injury, spinal cord injury, stroke, neurodegenerative diseases and some types of cancer. Therefore, it is considered a biomarker for these conditions.

A phagosome is a type of membrane-bound organelle that forms around a particle or microorganism following its engulfment by a cell, through the process of phagocytosis. This results in the formation of a vesicle containing the ingested material, which then fuses with another organelle called a lysosome to form a phago-lysosome. The lysosome contains enzymes that digest and break down the contents of the phagosome, allowing the cell to neutralize and dispose of potentially harmful substances or pathogens.

In summary, phagosomes are important organelles involved in the immune response, helping to protect the body against infection and disease.

Protein carbonylation is a post-translational modification of proteins, which involves the introduction of carbonyl groups (-CO) into amino acid side chains. This process can occur as a result of various reactive oxygen species (ROS) and oxidative stress, leading to the formation of protein adducts that can alter protein structure and function. Carbonylation can also be induced by advanced glycation end-products (AGEs), which are formed during non-enzymatic glycation reactions between reducing sugars and proteins. Protein carbonylation is often associated with aging, neurodegenerative diseases, and other pathological conditions characterized by oxidative stress and protein misfolding.

Nestin is a type of class VI intermediate filament protein that is primarily expressed in various types of undifferentiated or progenitor cells in the nervous system, including neural stem cells and progenitor cells. It is often used as a marker for these cells due to its expression during stages of active cell division and migration. Nestin is also expressed in some other tissues undergoing regeneration or injury.

The Ketoglutarate Dehydrogenase Complex (KGDC or α-KGDH) is a multi-enzyme complex that plays a crucial role in the Krebs cycle, also known as the citric acid cycle. It is located within the mitochondrial matrix of eukaryotic cells and functions to catalyze the oxidative decarboxylation of α-ketoglutarate into succinyl-CoA, thereby connecting the Krebs cycle to the electron transport chain for energy production.

The KGDC is composed of three distinct enzymes:

1. α-Ketoglutarate dehydrogenase (E1): This enzyme catalyzes the decarboxylation and oxidation of α-ketoglutarate to form a thioester intermediate with lipoamide, which is bound to the E2 component.
2. Dihydrolipoyl succinyltransferase (E2): This enzyme facilitates the transfer of the acetyl group from the lipoamide cofactor to CoA, forming succinyl-CoA and regenerating oxidized lipoamide.
3. Dihydrolipoyl dehydrogenase (E3): The final enzyme in the complex catalyzes the reoxidation of reduced lipoamide back to its disulfide form, using FAD as a cofactor and transferring electrons to NAD+, forming NADH.

The KGDC is subject to regulation by several mechanisms, including phosphorylation-dephosphorylation reactions that can inhibit or activate the complex, respectively. Dysfunction of this enzyme complex has been implicated in various diseases, such as neurodegenerative disorders and cancer.

It has been proved that in these neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and Huntington's disease ... Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease ... Alzheimer's disease and Huntington's disease. PCD observed in neurodegenerative diseases may be directly pathogenic; ... Alzheimer's disease (AD) is a chronic neurodegenerative disease that results in the loss of neurons and synapses in the ...
Disease: amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), Huntington's disease (HD), spinal muscular atrophy (SMA ... See the Motor Neuron Fact Sheet for details regarding other motor neuron diseases. Neurodegenerative diseases of the central ... Huntington's disease (HD), and Parkinson's disease (PD). These diseases are characterized by chronic and progressive neuronal ... Neurodegenerative diseases are a heterogeneous group of complex disorders linked by the degeneration of neurons in either the ...
Main classes of neurodegenerative diseases are Alzheimer's disease, Parkinson's disease, Huntington's disease and Amyotrophic ... These unexpected diseases hindered estrogen to get involved in neurodegenerative disease therapy. So, when applying estrogen- ... Neurodegenerative diseases are diseases caused along the process of neurodegeneration. Neurodegeneration includes structural ... Neurodegenerative diseases can disrupt the normal human homeostasis and result in abnormal estrogen levels. For example, ...
The German Center for Neurodegenerative Diseases (German: Deutsches Zentrum für Neurodegenerative Erkrankungen, (DZNE)) is an ... The center's declared aim is to develop new preventive and therapeutic approaches for neurodegenerative diseases. To accomplish ... interdisciplinary research institution that investigates neurodegenerative disease in all its facets. It is one of six "centers ... to combat the most important and widespread diseases. The DZNE is part of the Helmholtz Association of German Research Centres ...
Prion diseases, also called transmissible spongiform encephalopathies (TSEs), are neurodegenerative diseases of the brain ... Liberski PP (2012). "Gerstmann-Sträussler-Scheinker Disease". Neurodegenerative Diseases. Advances in Experimental Medicine and ... GSS is part of a group of diseases called transmissible spongiform encephalopathies. These diseases are caused by prions, which ... neurodegenerative disease that affects patients from 20 to 60 years in age. It is exclusively heritable, and is found in only a ...
Examples of neurodegenerative disorders include Alzheimer's disease, Parkinson's disease, and Huntington's disease. The focus ... including neurodegenerative disorders such as Parkinson's disease (PD) and Alzheimer's disease (AD), in rodent and non-human ... "Neurodegenerative Diseases". National Institute of Environmental Health Sciences. Retrieved 2019-02-27. (CS1 errors: periodical ... Neurodegenerative disorders are a result of neuronal loss of function over time which lead to cell death. ...
Neurodegenerative Disease. 5 (3-4): 261-263. doi:10.1159/000113719. PMID 18322407. v t e (Articles lacking in-text citations ... Moon, G.; Manktelow, T.C. (2002). "Cognitive deficits in recently diagnosed untreated patients with Parkinson's disease". ... disease (both physical and mental), medicines and drugs. The standard battery of cognitive tests in The CDR system includes ... Alzheimer's disease, and Vascular Dementia". Neurology. 54 (8): 1616-1625. doi:10.1212/WNL.54.8.1616. PMID 10762503. S2CID ...
"Parkinson's Disease". National Institute on Aging. Retrieved 2020-12-12. "Neurodegenerative Diseases". National Institute of ... It is the second most prevalent neurodegenerative disease, following Alzheimer's disease. It is estimated that nearly one ... Parkinson's disease is a neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra ... Animal models of Parkinson's disease are essential in the research field and widely used to study Parkinson's disease. ...
Hughes JR (2012). "The Savant Syndrome and Its Possible Relationship to Epilepsy". Neurodegenerative Diseases. Advances in ... Approximately half of savants are autistic; the other half often have some form of central nervous system injury or disease. It ...
Coyle JT (2017). "Schizophrenia: Basic and Clinical". Neurodegenerative Diseases. Advances in Neurobiology. Vol. 15. pp. 255- ... Stroke, multiple sclerosis, hyperthyroidism, hypothyroidism, and dementias such as Alzheimer's disease, Huntington's disease, ... autoimmune diseases, and cardiovascular diseases. The association of these with schizophrenia may be partially due to ... mind-split disease') to tōgō-shitchō-shō (統合失調症, lit. 'integration-dysregulation syndrome') to reduce stigma. The new name, ...
Takeda, N.; Kishimoto, Y.; Yokota, O. (2012). "Pick's Disease". Neurodegenerative Diseases. Advances in Experimental Medicine ... Pick's disease, also known as frontotemporal amnesia, is caused by atrophy of the frontotemporal lobe. Emotional symptoms ... "Clinicopathological characterization of Pick's disease versus frontotemporal lobar degeneration with ubiquitin/TDP-43-positive ...
397-. ISBN 978-3-642-02912-7. Dominguez C (18 November 2010). Neurodegenerative Diseases. Springer Science & Business Media. pp ... gastroesophageal reflux disease, and dental anxiety. It reached phase II clinical trials for all of the aforementioned ...
In neurodegenerative diseases, cells of the central nervous system stop working or die via neurodegeneration. An example of ... Alzheimer's disease (AD) Amyotrophic lateral sclerosis (ALS, Lou Gehrig's disease) Cancers Charcot-Marie-Tooth disease (CMT) ... coronary artery disease) and neoplastic diseases (e.g. cancers). Many degenerative diseases exist and some are related to aging ... "Neurodegenerative Diseases". Archived from the original on 2018-07-28. Retrieved 2018-09-17. Nopoulos, PC (2016). "Huntington ...
Guam disease, or amyotrophic lateral sclerosis-parkinsonism-dementia (ALS-PDC) is a neurodegenerative disease of uncertain ... Parkinson's disease, and Alzheimer's disease. First reports of the disease surfaced in three death certificates on Guam in 1904 ... The disease was shown to be familial but not genetic. Chamorro who grew up outside of Guam had not developed the disease, and ... Holtcamp W (March 2012). "The emerging science of BMAA: do cyanobacteria contribute to neurodegenerative disease?". Environ. ...
... and its spread throughout the brain makes Parkinson's disease a neurodegenerative disease classed as a synucleinopathy, and ... Parkinson's disease dementia becomes common in advanced stages of the disease. The motor symptoms of the disease result from ... Parkinson's disease, Aging-associated diseases, Ailments of unknown cause, Geriatrics, Neurodegenerative disorders, ... Some autoimmune diseases may even increase one's risk of developing PD, up to 33% in one study. Autoimmune diseases linked to ...
Neurodegenerative Diseases. 8 (5): 375-380. doi:10.1159/000324373. ISSN 1660-2862. PMC 3121545. PMID 21389683. Huang, S.; ... chronic kidney disease,HIV-1 disease,tick-borne encephalitis and Lyme,malaria,hepatitis, burns,multiple organ dysfunction ... Decreased levels are often associated with ill health and disease. A growing list of insults showing loss of pGSN includes ... Ji, Lina; Zhao, Xi; Hua, Zichun (2015-01-06). "Potential Therapeutic Implications of Gelsolin in Alzheimer's Disease". Journal ...
Kaether C, Haass C, Steiner H (2006). "Assembly, trafficking and function of gamma-secretase". Neuro-Degenerative Diseases. 3 ( ... Alzheimer's disease, Proteins, All stub articles, Human chromosome 19 gene stubs). ...
Neuro-Degenerative Diseases. 4 (5): 366-75. doi:10.1159/000105157. PMID 17622779. S2CID 9020464. Lescuyer P, Allard L, ... who have found emerging evidence that indicates a role in differentiating between different neurodegenerative diseases. To ... is decreased in brains of patients with Down syndrome and Alzheimer's disease". Advances in Down Syndrome Research. pp. 225-34 ...
Neurodegenerative Disease Management. 9 (1): 5-23. doi:10.2217/nmt-2018-0033. ISSN 1758-2024. PMID 30480471. "Onpattro ( ... "FDA approves first-of-its kind targeted RNA-based therapy to treat a rare disease" (Press release). U.S. Food and Drug ... Lipschultz B, Cortez M (10 August 2018). "Rare-Disease Treatment From Alnylam to Cost $450,000 a Year". Bloomberg. Archived ... a fatal rare disease that is estimated to affect 50,000 people worldwide. It is the first small interfering RNA-based drug ...
Neurodegenerative Disease Management. 11 (5): 411-429. doi:10.2217/nmt-2020-0066. PMID 34472379. S2CID 237389009. Morales- ... Eventually the disease can affect other muscles such as the ones located in the face. By definition, LGMDs primarily affect ... The disease commonly leads to dependence on a wheelchair within years of symptom onset, although some patients maintain ... Limb-girdle muscular dystrophy is explained in terms of gene, locus, OMIM and type as follows: For a disease entity to be ...
Shen J (2 October 2013). "Function and dysfunction of presenilin". Neuro-Degenerative Diseases. 13 (2-3): 61-3. doi:10.1159/ ... Smialowska A, Baumeister R (2006). "Presenilin function in Caenorhabditis elegans". Neuro-Degenerative Diseases. 3 (4-5): 227- ... An important part of the disease process in Alzheimer's disease is the accumulation of Amyloid beta (Aβ) protein. To form Aβ, ... Most cases of Alzheimer's disease are not hereditary. However, there is a small subset of cases that have an earlier age of ...
Neurodegenerative Disease Management. 2 (6): 561-564. doi:10.2217/nmt.12.64. Laws, Keith R; Stoet, Gijsbert; O'Connor, Daryl B ... Laws, Keith R; Irvine, Karen (December 2012). "Do women with Alzheimer's disease demonstrate greater cognitive deterioration ... "Greater cognitive deterioration in women than men with Alzheimer's disease: a meta analysis". Human Psychopharmacology: ... in patients with schizophrenia and to demonstrate worse cognitive outcomes in women suffering from Alzheimer's disease. Laws' ...
Neuro-Degenerative Diseases. 7 (1-3): 170-174. doi:10.1159/000289231. ISSN 1660-2862. PMC 2859236. PMID 20197700. Murray, ... such as Alzheimer's disease and cerebrovascular disease(s). LATE has a large impact on public health. Clinical-pathologic ... In these persons, the presence of LATE-NC is associated with a swifter disease course and with more severe clinical (memory and ... In other words, the symptoms of LATE are similar to those of Alzheimer's disease. The acronym LATE stands for Limbic- ...
2002). "Is the saitohin gene involved in neurodegenerative diseases?". Ann. Neurol. 52 (6): 829-32. doi:10.1002/ana.10384. PMID ... Neuro-Degenerative Diseases. 2 (1): 28-35. doi:10.1159/000086428. PMID 16909000. S2CID 6644618. v t e (Articles with short ... which is nested in the tau locus and confers allele-specific susceptibility to several neurodegenerative diseases, interacts ... which is nested in the tau locus and confers allele-specific susceptibility to several neurodegenerative diseases, interacts ...
... voice and language in Parkinson's disease: Changes and interventions". Neurodegenerative Disease Management. 2 (3): 279-289. ... Parkinson's disease is a chronic neurodegenerative disorder that involves the loss of dopaminergic neurons in the brain. While ... They have concluded that patients with Parkinson's disease tend to struggle with specific areas of prosody; they are less able ... The degradation of prosody in Parkinson's disease over time is independent of motor control issues, and is thus separate from ...
May 2020). "A novel neurodegenerative spectrum disorder in patients with MLKL deficiency". Cell Death & Disease. 11 (5): 303. ... Schippling S (November 2017). "MRI for multiple sclerosis diagnosis and prognosis". Neurodegenerative Disease Management. 7 (6s ... Schilder disease or diffuse myelinoclastic sclerosis: is a rare disease that presents clinically as a pseudotumoural ... As of 2019, three auto-antibodies have been found in atypical MS giving birth to separate diseases: Anti-AQP4 diseases, Anti- ...
Neuro-Degenerative Diseases. 11 (3): 129-40. doi:10.1159/000336427. PMID 22626981. S2CID 46024586. Giménez-Llort L, Ratia M, ... In animal studies it has nootropic and neuroprotective effects, and is used in research into Alzheimer's disease, and although ... "Huprine X is a novel high-affinity inhibitor of acetylcholinesterase that is of interest for treatment of Alzheimer's disease ... "Huprine X and huperzine A improve cognition and regulate some neurochemical processes related with Alzheimer's disease in ...
February 2016). "Emerging therapies in Friedreich's ataxia". Neurodegenerative Disease Management. 6 (1): 49-65. doi:10.2217/ ... Best practice in rare diseases". Orphanet Journal of Rare Diseases. 17 (1): 415. doi:10.1186/s13023-022-02568-3. PMC 9652828. ... The disease primarily affects the spinal cord and peripheral nerves. The spinal cord becomes thinner and nerve cells lose some ... The disease evolves differently in different people. In general, those diagnosed at a younger age or with longer GAA triplet ...
... as well as diseases such as neurodegenerative diseases, atherosclerosis, and cancer. To elaborate, LRP1 mainly contributes to ... and diseases, such as neurodegenerative diseases, atherosclerosis, and cancer. The LRP1 gene encodes a 600 kDa precursor ... Neuro-Degenerative Diseases. 11 (1): 13-21. doi:10.1159/000337231. ISSN 1660-2862. PMID 22572854. S2CID 30189180. Bachmeier, ... In support of this, LRP1 expression is reduced in endothelial cells as a result of normal aging and Alzheimer's disease in ...
"Clinical pharmacology review of safinamide for the treatment of Parkinson's disease". Neurodegenerative Disease Management. 5 ( ... Safinamide (INN; brand name Xadago) xinafact 50 mg is a drug used as an add-on treatment for Parkinson's disease with "off" ... Safinamide is used to treat idiopathic Parkinson's disease as add-on for people taking a stable dose of levodopa (L-dopa) alone ... "Study of Safinamide in Early Parkinson's Disease as Add-on to Dopamine Agonist (MOTION)". PDtrials.org. Archived from the ...
It has been proved that in these neurodegenerative diseases (Alzheimers disease, Parkinsons disease, and Huntingtons disease ... Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinsons disease, Alzheimers disease ... Alzheimers disease and Huntingtons disease. PCD observed in neurodegenerative diseases may be directly pathogenic; ... Alzheimers disease (AD) is a chronic neurodegenerative disease that results in the loss of neurons and synapses in the ...
Events in the brain during the evolution of Alzheimers disease Alzheimers disease is a complex and chronic disease that ... Neurodegenerative diseases are a heterogeneous group of disorders that are characterized by the progressive degeneration of the ... Cost-effective Alzheimers disease detection using plasma p-tau217-based risk stratification Cost-effective and scalable means ... A meta-analysis identifies factors predicting the future development of freezing of gait in Parkinsons disease *Talia Herman ...
... that causes them to kick or cry out during their sleep may be at greater risk of developing dementia or Parkinsons disease, ... High risk of neurodegenerative disease. The study showed that the chance a patient suffering from an REM sleep behaviour ... Sleep Disorders: Warning Sign For Neurodegenerative Disease?. Date:. December 29, 2008. Source:. McGill University Health ... REM sleep behavior disorder appears to be a predictor of neurodegenerative disease in more than 50 percent of cases. ...
"What kills neurons in neurodegenerative diseases?", a review series in an open access journal Authors: Todd E Golde and Leonard ... What have worm models told us about the mechanisms of neuronal dysfunction in human neurodegenerative diseases? The nematode ... Does neuroinflammation fan the flame in neurodegenerative diseases? While peripheral immune access to the central nervous ... Alzheimers disease: synaptic dysfunction and Aβ Synapse loss is an early and invariant feature of Alzheimers disease (AD) and ...
... is committed to finding treatments and cures to improve the lives of patients with neurodegenerative disorders including ... Institute for Neurodegenerative Disease. Mass General Institute for Neurodegenerative Disease (MIND) is committed to finding ... Diseases We Research MIND studies neurodegenerative disorders, most importantly Parkinsons, Huntingtons, Alzheimers and ALS ... Alzheimers disease, Huntingtons disease and Parkinsons disease. ...
... the malformed proteins that lead to the disease. ... have developed a novel strategy for tackling neurodegenerative ... diseases such as Huntingtons disease: encouraging an individuals own cells to eat ... Neurodegenerative Disease, Neurodegenerative Diseases, Neuron, Neurons, Protein, Rapamycin, Research, Small Molecules, T-Cell, ... Scientists have developed a novel strategy for tackling neurodegenerative diseases such as Huntingtons disease: encouraging an ...
... imaging and its potential in neurodegenerative disease research. ... Metabolic Imaging in Neurodegenerative Disease using CEST MRI. ... This Webinar is of interest to researcher and professionals working in the field of neurodegenerative diseases including people ... imaging and its potential in neurodegenerative disease research. ... How microCT Can Provide Insight into Dynamic Disease Processes ... Unlocking your clinical understanding of Post-Acute COVID Syndrome (PACS), patient recover, and risk of subsequent disease ...
Women should increase consumption of lutein and zeaxanthin-rich food to reduce incidence of age-related diseases, such as ... Carotenoid intake may help reduce neurodegenerative disease in women. By Nicola Gordon-Seymour 25-Jul-2022. - Last updated on ... help ameliorate characteristic co-morbidities associated with age-related neurodegenerative diseases, like oxidative and ... Although women generally live longer than men, they are much more likely to suffer from age-related disease and disability, ...
Advancing knowledge of human development, developmental disabilities, and neurodegenerative diseases.
Prion Diseases. Prion diseases are a group of severe neurodegenerative diseases that are caused by misfolded prion proteins. ... The Essential GuideHeart DiseaseParkinsons DiseaseCancerTinnitusArthritisAlzheimers DiseaseAnxietyMigrainesKidney Disease ... Many neurodegenerative diseases have been linked to specific proteins that have prion-like properties, and these diseases are ... Parkinsons disease is the second most common neurodegenerative disorder and the most common neurodegenerative motor disorder. ...
... are now recognized as a constant pathological hallmark of various neurodegenerative diseases including amyotrophic lateral ... sclerosis (ALS), Parkinson, Alzheimer, Huntington and prion diseases (Fan et al. 2008). In ALS, structural Golgi alterations ... and mechanistic descriptions of the major neurodegenerative diseases including Parkinson disease (Wang and Hay), Alzheimer ... 2008). Golgi apparatus and neurodegenerative diseases. Int. J. Dev. Neurosci. 26, 523-534. doi: 10.1016/j.ijdevneu.2008.05.006 ...
... yet the chronic neurodegenerative disease has no cure or effective treatment. ... Alzheimers disease is the sixth leading cause of death among U.S. adults, ... Alzheimers disease is the sixth leading cause of death among U.S. adults, yet the chronic neurodegenerative disease has no ... Student-developed algorithm takes aim at neurodegenerative disease. June 8, 2017. ScienceBlog.com ...
Multiple Bioactivities of Traditional Medicinal Herbs for Treatment of Neurodegenerative Diseases - A Special Issue published ... Parkinsons disease (PD), another common neurodegenerative disease prevalent among the elderly, affects 1-3% of the population ... Age-related dementia constitutes a major subset of neurodegenerative disease. Alzheimers disease (AD) is the most prevalent ... 80 years by 2050 to have a neurodegenerative disease. Owing to the financial, societal, and personal impact of these diseases, ...
The annual worldwide cost of Alzheimer
Despite this, the genetic basis of the disorder is not well defined and its boundaries with other neurodegenerative diseases ... Analysis of neurodegenerative disease-causing genes in dementia with Lewy bodies Acta Neuropathol Commun. 2020 Jan 29;8(1):5. ... Despite this, the genetic basis of the disorder is not well defined and its boundaries with other neurodegenerative diseases ... 9 Department of Medicine, Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada. ...
We annotated targets and eligibility criteria for 3238 neurodegenerative disease trials registered at ClinicalTrials.gov from ... The potential for disease modification through early intervention against root molecular causes of disease remains largely ... Though often linked to disease initiation, not progression, these targets were tested mostly at symptomatic disease stages. ... Engaging the right target, at the right disease stage, could be an important determinant of success. ...
Levodopa-Carbidopa Gel Safely Reduces Parkinsons Disease Tremors Patients with advanced Parkinsons disease had resting ... Parkinsons disease (PD) "off"-period symptoms control is better following administration of an inhaled levodopa powder ... For patients with moderate to severe Alzheimers disease, adding memantine to cholinesterase inhibitor treatment can improve ... Close more info about Levodopa-Carbidopa Gel Safely Reduces Parkinsons Disease Tremors ...
... and treatment of various neurodegenerative and cardiovascular diseases in humans. Keywords: apolipoprotein E, pathogenesis, ... s disease, cardiovascular diseases, multiple sclerosis, type 2 diabetes mellitus, Type III hyperlipoproteinemia, vascular ... This review will summarize the updated research progress on APOE functions and its role in Alzheimer’s disease, Parkinson ... and their isoforms is important to determine its role in various diseases and to advance the development of therapeutic ...
Innate immunity in chronic neurodegenerative disease. Add to your list(s) Download to your calendar using vCal ... Michael Heneka will be talking about the innate immune response of microglia in neurodegenerative diseases. He has published ... University of Cambridge , Talks.cam , Microglia webinar series , Innate immunity in chronic neurodegenerative disease ... extensively on microglia, neuroinflammation and Alzheimers disease including:. mTOR-dependent translation amplifies microglia ...
Center for Neurodegenerative Disease Research. Center for Neurodegenerative Disease Research. Perelman School of Medicine at ... More recently, the team has shown, first in Parkinsons, how pathology spreads from cell-to-cell in neurodegenerative diseases ... and prevention of neurodegenerative diseases - and to translate progress in the lab to clinical practice. Researchers pursue a ... other Motor Neuron Diseases. Virginia M.-Y. Lee, PhD, MBA and John Q. Trojanowski, MD, PhD founded and co-directed CNDR until ...
The Wasserman family has experienced first-hand the devastating effects of neurodegenerative diseases: Sandra Wasserman lost ... "Alex was looking at neurodegenerative diseases with new eyes and a whole different vision that was exciting to me," Sandra ... Through Project ALS, the Wasserman family saw an important opportunity to guide and directly impact neurodegenerative disease ... The Wasserman family has experienced first-hand the devastating effects of neurodegenerative diseases: Sandra Wasserman lost ...
... the molecular mechanisms underlying these diseases are still poorly understood, and effective drug treatments are generally ... Neurodegenerative and neurodevelopmental diseases constitute a major health burden, and in spite of several decades of ... including the diseases we will study in this proposal: Alzheimers disease, prion disease, Parkinsons disease, Charcot-Marie- ... Neurodegenerative and neurodevelopmental diseases constitute a major health burden, and in spite of several decades of ...
KIF1A neurodegenerative disease mutations modulate motor motility and force generation. Dipeshwari J. Shewale, View ORCID ... KIF1A neurodegenerative disease mutations modulate motor motility and force generation Message Subject (Your Name) has ... Several point mutations in the KIF1A motor domain have been identified in patients with various motor neuron diseases. Recent ... The observed changes in motility properties and cargo transport align with the severity of disease phenotype observed in KIF1A- ...
The European Platform for Neurodegenerative Diseases (EPND) integrates existing initiatives to build, grow, and deliver a ... Members of the European Platform for Neurodegenerative Diseases (EPND) announced today that they will embark on a venture to ... New European initiative will build a collaborative platform for data and sample sharing for neurodegenerative diseases. The ... EPND will bring together the neurodegenerative disease community across Europe, securing the legacy of many siloed initiatives ...
John Hardy on Similarities between prion diseases and other neurodegenerative diseases, part of a collection of multimedia ... Similarities between prion diseases and other neurodegenerative diseases. *Prof. John Hardy - Institute of Neurology, ... Similarities between prion diseases and other neurodegenerative diseases. Embed in course/own notes ... Hardy, J. (2008, September 4). Similarities between prion diseases and other neurodegenerative diseases [Video file]. In The ...
... and eventually neurodegenerative disease. Preventative medicine should start at the top, well before onset of neurodegenerative ... "The good thing is these are variables we can control," said Perlmutter, "which is especially good for a disease that has no ... These studies summarize Perlmutters idea that age-related disease prevention should start as early as possible. For this, he ... The pharmaceutical industry is losing its battle in terms of developing a magic bullet for Alzheimers disease. The answer is ...
This study describes the 127 children with neurodegenerative disease who were admitted to Helen House, a hospice for children, ... Little is written on the management of problems encountered by children with neurodegenerative disease. Whilst the conditions ... are individually rare, as a group of diseases they pose a considerable burden on the child, the family and the community. ...
Microtubule motors and axonal transport : function and dysfunction in neurodegenerative disease / Erika Holzbaur. ... Health and Aging Trajectories: Shared and Competing Risks and Resiliencies for Chronic Diseases Associated with Aging (Day 1) ... NIH State-of-the-Science Conference: Preventing Alzheimers Disease and Cognitive Decline - Day 1 ... exploring the link between defects in axonal transport and the development of neuropathogenesis in degenerative diseases such ...
Parkinson disease. We standardized the Lyme disease incidence rates and neurodegenerative disease death rates to the 2000 US ... Associations between Lyme disease and certain neurodegenerative diseases have been proposed, but supportive evidence for an ... We compared Lyme disease incidence rates in each state with death rates for Alzheimer disease, ALS, MS, and Parkinson disease. ... If Lyme disease was etiologically linked to Alzheimer disease, ALS, MS, or Parkinson disease, rates of death attributed to ...
  • Neurodegenerative diseases are a heterogeneous group of disorders that are characterized by the progressive degeneration of the structure and function of the central nervous system or peripheral nervous system. (nature.com)
  • Sleep Disorders: Warning Sign For Neurodegenerative Disease? (sciencedaily.com)
  • These results establish a clear link and indicate that these sleep disorders could be a predictor of neurodegenerative disease," explained Dr. Postuma. (sciencedaily.com)
  • Prion diseases are disorders of protein conformation in which PrP C , the normal cellular conformer, is converted to an abnormal, protease-resistant conformer rPrP Sc . (biomedcentral.com)
  • α-Synuclein is a small protein that has special relevance for understanding Parkinson disease and related disorders. (biomedcentral.com)
  • Despite major advances in our understanding of the initiating factors that trigger many neurodegenerative disorders, to date, no novel disease-modifying therapies have been shown to provide significant benefit. (biomedcentral.com)
  • Mass General Institute for Neurodegenerative Disease (MIND) is committed to finding treatments to improve the lives of patients with neurodegenerative disorders like ALS, Alzheimer's disease, Huntington's disease and Parkinson's disease. (massgeneral.org)
  • Our paper showed that there are several mechanisms by which these vaccines could lead to severe disease , including autoimmune disease, neurodegenerative diseases, vascular disorders (hemorrhaging and blood clots) and possibly reproductive issues. (theepochtimes.com)
  • Thus, we invite investigators to contribute brief and original articles on neurodegenerative diseases via multiple bioactivities and the potential therapeutic effects of medicinal herbs on these disorders. (hindawi.com)
  • We analyzed variants in 60 genes implicated in DLB, Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and atypical parkinsonian or dementia disorders, in order to determine their frequency in DLB. (nih.gov)
  • CNDR scientists collaborate with researchers not only at Penn, but also from institutions around the globe to find better ways to diagnose and treat neurodegenerative disorders. (upenn.edu)
  • Since its founding, CNDR has contributed to a dramatic expansion in basic and clinical research programs on neurodegenerative disorders at Penn. (upenn.edu)
  • Alterations in protein synthesis have been implicated in several of these diseases, including the diseases we will study in this proposal: Alzheimer's disease, prion disease, Parkinson's disease, Charcot-Marie-Tooth disease and autism spectrum disorders. (alzheimer-europe.org)
  • There is currently a lack of available treatments that can prevent or modify the progression of neurodegenerative disorders like Alzheimer's disease (AD) and Parkinson's disease (PD), which affect millions of people in Europe. (kcl.ac.uk)
  • Because of the neurotropism of Lyme disease, speculative websites and articles and even peer-reviewed journals have purported causal associations between Lyme disease and several neurodegenerative disorders, including Alzheimer disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and Parkinson disease ( 6 - 11 ). (cdc.gov)
  • We hypothesized that, if there is a link between B. burgdorferi infection and subsequent development of Alzheimer disease, ALS, MS, or Parkinson disease, the geographic distribution of these neurodegenerative disorders should correlate with that of Lyme disease. (cdc.gov)
  • To determine if such a correlation exists, we compared the distribution of confirmed cases of Lyme disease in the United States with the distribution of deaths due to these 4 neurodegenerative disorders. (cdc.gov)
  • We used the Moran's I test for spatial autocorrelation to assess geographic clustering of state incidence rates of Lyme disease and of death rates for the 4 neurologic disorders by using ArcGIS 10.1 (ESRI, Redlands, CA, USA). (cdc.gov)
  • Furthermore, the research team found that curli also promoted neurodegeneration in animal models of Alzheimer's disease, Amyotrophic lateral sclerosis, and Huntington's disease, suggesting that the bacteria-secreted curli may have detrimental effects in a range of neurodegenerative disorders. (hku.hk)
  • Neurodegenerative diseases (NDDs) are devastating disorders which impair memory, cognition, movements, and general functioning. (aao.org)
  • It stands to reason, therefore, that neurodegenerative disorders might also cause degeneration of neurons in the retina. (aao.org)
  • Background Several studies suggest that multiple rare genetic variants in genes causing monogenic forms of neurodegenerative disorders interact synergistically to increase disease risk or reduce the age of onset, but these studies have not been validated in large sporadic case series. (bmj.com)
  • Some of those issues could include neurodegenerative disorders, which researchers believe further research may show. (scitechdaily.com)
  • These aptamers could be used to study, at the molecular level , the phenomenon of abnormal protein aggregation typical of several neurodegenerative diseases and would, therefore, pave the way for the development of early diagnosis tools for these disorders. (phys.org)
  • Neurodegenerative disorders present some of the biggest challenges in planning and conducting clinical drug trials. (premier-research.com)
  • Dr. Postuma is a leading researcher in movement disorders and also the head of an international collaboration which received a US$35 million grant from the National Institutes of Health in the US to identify biomarkers for people with REM Sleep Behaviour Disorder, a precursor of several neurological diseases including Parkinson's. (mcgill.ca)
  • There are over 100,000 Canadians living with Parkinson's, a neurodegenerative disease in which the cells that normally produce dopamine (which helps control movement) die off, resulting in tremors, impaired balance and muscle rigidity as well as many non-motor symptoms such as cognitive changes and mood disorders. (mcgill.ca)
  • However, the extent to which 'network-based neurodegeneration' applies across the wide range of neurodegenerative disorders remains unclear. (lu.se)
  • Lysosomal storage diseases describe a heterogeneous group of dozens of rare inherited disorders characterized by the accumulation of undigested or partially digested macromolecules, which ultimately results in cellular dysfunction and clinical abnormalities. (medscape.com)
  • Lysosomal storage diseases are generally classified by the accumulated substrate and include the sphingolipidoses, oligosaccharidoses, mucolipidoses, mucopolysaccharidoses (MPSs), lipoprotein storage disorders, lysosomal transport defects, neuronal ceroid lipofuscinoses and others. (medscape.com)
  • Accumulated data indicate that hematopoietic stem cell transplantation may be effective under optimal conditions in preventing the progression of central nervous system symptoms in neuronopathic forms of lysosomal storage diseases (such as Krabbe disease), including some of the mucopolysaccharidoses, oligosaccharidoses, sphingolipidoses, and lipidoses as well as peroxisome disorders such as X-linked adrenoleukodystrophy. (medscape.com)
  • In general, transplantation yields the best results when performed early in the course of the disease (ie, in an asymptomatic affected sibling of a child with a lysosomal storage disorder), in centers with experience in performing transplantations to treat inherited metabolic disorders, and in patients healthy enough to tolerate the conditioning and transplantation regimen. (medscape.com)
  • Two new studies have provided important mechanistic insights into TDP-43 pathology, a hallmark of neurodegenerative conditions such as amyotrophic lateral sclerosis and frontotemporal lobar degeneration. (nature.com)
  • [10] It has already described abnormalities in Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and multiple sclerosis among others. (aao.org)
  • Methods We analysed 980 neuropathologically characterised human brains with Alzheimer's disease (AD), Parkinson's disease-dementia with Lewy bodies (PD-DLB), frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) and age-matched controls. (bmj.com)
  • A team of researchers from the IIT-Istituto Italiano di Tecnologia (Italian Institute of Technology) has designed in silico "molecular probes" able to track the progress of a protein that misbehaves in different neurodegenerative diseases, such as Amyotrophic Lateral Sclerosis (ALS) and Fronto-Temporal Dementia (FTD). (phys.org)
  • Early pathogenesis in the adult-onset neurodegenerative disease amyotrophic lateral sclerosis. (umassmed.edu)
  • This supports a new concept that beyond splicing caused by the gene mutation, RBM20 is an RNA-binding protein granule disease similar to diseases like Lou Gehrig's disease, or amyotrophic lateral sclerosis, and Alzheimer's disease. (devdiscourse.com)
  • Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a progressive, fatal neurodegenerative disorder that causes the loss of motor neurons, typically resulting in paralysis, respiratory failure, and death within 3-5 years of symptom. (cdc.gov)
  • Extensive genetic, biochemical, and histological evidence has implicated the amyloid-β peptide (Aβ) in Alzheimer's disease pathogenesis, and several mechanisms have been suggested, such as metal binding, react. (biomedcentral.com)
  • While numerous hypotheses have been proposed to explain the molecular mechanisms underlying the pathogenesis of neurodegenerative diseases, the theory of oxidative stress has received considerable support. (biomedcentral.com)
  • The pathogenesis of neurodegenerative diseases remains unclear and the present one-drug, one-target paradigm for treating neurodegenerative diseases appears clinically unsuccessful. (hindawi.com)
  • CNDR provides leadership, training/education, and core support to augment and enhance ongoing collaborative studies as well as to stimulate new investigations into the etiology, pathogenesis, diagnosis, treatment, and prevention of neurodegenerative diseases - and to translate progress in the lab to clinical practice. (upenn.edu)
  • Studies in the last few years have suggested that gut bacteria may play an important role in the pathogenesis of neurodegenerative diseases. (hku.hk)
  • For example, neuropathological investigations of Alzheimer's disease pathogenesis can fall in disagreement with conclusions reached by biomarker -based investigations. (bvsalud.org)
  • Occupations with statistically significant increased proportionate mortality for deaths occurring between the ages of 15 and 55yr were also examined since a relatively early age at death might indicate that an occupational factor was involved in the etiology or pathogenesis of the diseases. (cdc.gov)
  • Find out how microplate readers advance research into mitochondrial dysfunction and different neurodegenerative diseases. (bmglabtech.com)
  • However, when mitochondria fail to function properly different neurodegenerative diseases can take hold. (bmglabtech.com)
  • Relevance of biomarkers across different neurodegenerative diseases. (bvsalud.org)
  • Here, we discuss themes of biomarker use in neurodegenerative disease research , commenting on appropriate use, interpretation, and considerations for implementation across different neurodegenerative diseases . (bvsalud.org)
  • Within neurodegenerative diseases, it is estimated that 55 million people worldwide had dementia in 2019, and that by 2050 this figure will increase to 139 million people. (wikipedia.org)
  • People with a sleep disorder that causes them to kick or cry out during their sleep may be at greater risk of developing dementia or Parkinson's disease, according to a new study. (sciencedaily.com)
  • Doctors should pay close attention when following these patients, as their observations could help define the precursors of diseases such as Parkinson's, Alzheimer's, Lewy body dementia, or multiple system atrophy," stated Dr. Montplaisir, principal investigator of the study. (sciencedaily.com)
  • Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia. (biomedcentral.com)
  • Women should increase consumption of lutein and zeaxanthin-rich food to reduce incidence of age-related diseases, such as macular degeneration and dementia, according to experts. (nutraingredients.com)
  • They are known to improve cognitive function and prevent central nervous system degeneration, as well as protecting the retina from blue glare damage that precedes neurogenerative disease, like age-related macular degeneration and some forms of dementia. (nutraingredients.com)
  • Age-related dementia constitutes a major subset of neurodegenerative disease. (hindawi.com)
  • Alzheimer's disease (AD) is the most prevalent clinical form of dementia in aging populations, and 43% of individuals aged ≥ 85 years are thought to have AD in the United States. (hindawi.com)
  • This review will summarize the updated research progress on APOE functions and its role in Alzheimer's disease, Parkinson's disease, cardiovascular diseases, multiple sclerosis, type 2 diabetes mellitus, Type III hyperlipoproteinemia, vascular dementia, and ischemic stroke. (dovepress.com)
  • 3 In this review, we discuss the biological functions of human APOE and its role in Alzheimer's disease (AD), Parkinson's disease (PD), cardiovascular diseases (CVD), multiple sclerosis (MS), type 2 diabetes mellitus (T2DM), vascular dementia (VD), and ischemic (occlusive) stroke (IS). (dovepress.com)
  • This programme will build a secure platform via a European node on the AD Workbench of the Alzheimer's Disease Data Initiative (ADDI), a medical research organisation committed to increasing interoperability of data platforms and empowering scientists to analyse data for new discoveries in dementia research. (kcl.ac.uk)
  • Apply for funding to work with researchers in Japan in the fields of neuroscience, neurodegenerative diseases and dementia. (ukri.org)
  • This opportunity aims to support research projects that address major questions in the fields of neuroscience, neurodegenerative disease and dementia, leveraging strengths of researchers in both the UK and Japan. (ukri.org)
  • understanding the underpinning mechanisms of neurodegenerative disease and dementia, and associated mental health conditions. (ukri.org)
  • Our ageing society is confronted with a dramatic increase in patients suffering from tauopathies such as Alzheimer's disease, frontotemporal dementia and others. (karger.com)
  • OSA is common in patients with dementia and the risk of Alzheimer's disease and vascular dementia may be increased in patients with OSA. (brainfoundation.org.au)
  • With no effective treatments for Alzheimer's disease currently available, identification and treatment of medical and lifestyle factors that contribute to dementia is currently the only option for reducing the prevalence and impact of this disease. (brainfoundation.org.au)
  • Neurodegenerative diseases are the most common cause of dementia. (lu.se)
  • Lifetime risks of developing Alzheimer's disease dementia vary considerably by age, gender and the presence of any signs or symptoms of dementia, a new study by Alzheimer's & Dementia: The Journal of the Alzheimer's Association reports. (neurodegenerationresearch.eu)
  • That same 65-year-old with amyloid plaques has a 10-year risk of Alzheimer's disease dementia of 2.5 percent. (neurodegenerationresearch.eu)
  • The authors state that the lifetime and 10-year risks are an indication of the potential that someone will develop Alzheimer's disease dementia based on their age and screenings for amyloid deposits, neurodegeneration and presence or absence of MCI or any combination of those three. (neurodegenerationresearch.eu)
  • Multiple neuropathologic processes may underlie dementia , including both neurodegenerative diseases and vascular disease. (medscape.com)
  • [ 2 ] All dementia share common molecular mechanisms responsible for disease etiology and progression, such as hypoxia and oxidative stress, neuroinflammation, mitochondrial bioenergetics, neurodegeneration, and blood-brain barrier permeability. (medscape.com)
  • Alzheimer disease (AD) is the most common neurodegenerative disease responsible for dementia. (medscape.com)
  • Mortality from presenile dementia (PSD), Alzheimer's disease (AD), Parkinson's disease (PD), and motor neuron disease (MND) was examined for 27 states in the National Occupational Mortality Surveillance (NOMS) system for the period 1982 through 1991. (cdc.gov)
  • Genetic variation in over 50 genes contributes to the risk of developing neurodegenerative diseases. (bmj.com)
  • Huntington's disease (HD) is a rare autosomal dominant neurodegenerative disorder caused by mutations in the huntingtin gene (HTT). (wikipedia.org)
  • Scientists have developed a novel strategy for tackling neurodegenerative diseases such as Huntington's disease: encouraging an individual's own cells to "eat" the malformed proteins that lead to the disease. (news-medical.net)
  • Huntington's disease is one of a number of degenerative diseases marked by clumps of malformed protein in brain cells. (news-medical.net)
  • The gene responsible for the disease was discovered in 1993, leading to a better understanding of the condition and to improved predictive genetic testing, but it has yet to lead to any treatments that slow the neurodegeneration in Huntington's patients. (news-medical.net)
  • Professor David Rubinsztein, a Wellcome Trust Senior Clinical Fellow at the University of Cambridge, has been studying the molecular biology underlying Huntington's and other neurodegenerative diseases. (news-medical.net)
  • In March alone, Takeda has agreed to pay up to $120 million in upfront fees and preclinical research milestones to work with Anima Biotech on molecules against hard-to-drug proteins, starting with a Huntington's disease program, and put up $196 million to regain the rights to an epilepsy drug from Ovid. (fiercebiotech.com)
  • 16 Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Perelman School of Medicine at the University of Pennsylvania, 3600 Spruce Street, Philadelphia, USA. (nih.gov)
  • In many papers, the pathological effects of neurodegenerative diseases are a result of altered activity in multiple pathways. (hindawi.com)
  • The Wasserman family has experienced first-hand the devastating effects of neurodegenerative diseases: Sandra Wasserman lost her beloved husband to Parkinson's disease, and her son to glioblastoma. (projectals.org)
  • Success has been particularly limited in adult-onset neurodegenerative diseases, for which no disease-modifying drug yet exists. (nature.com)
  • As with many neurodegenerative diseases, both rare autosomal-dominant forms of AD and more common sporadic forms with genetic risk factors without causative mutations exist. (medscape.com)
  • However, while misfolded protein aggregation clearly plays a role in neurodegenerative disease, this is evidently only a signature of neuronal damage and additional causative factors remain to be discerned. (hindawi.com)
  • The presentation titled 'Extracellular vesicles and their role in neurodegenerative diseases' covered a series of landmark studies investigating EVs and their role in spreading disease-associated proteins, and the diagnostic potential of EV miRNA profiles for the diagnosis of neurodegenerative diseases. (izon.com)
  • Growing evidence indicates that gut microbiota plays a critical role in regulating the progression of neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD), but the molecular mechanism underlying such microbe-host interaction is still unclear. (hku.hk)
  • The Dominantly Inherited Alzheimer Network (DIAN) unites researchers aiming to understand autosomal dominant Alzheimer's disease (ADAD). (nature.com)
  • Proteomic analysis of cerebrospinal fluid from people with dominantly inherited forms of the disease reveals the temporal progression of pathological changes in Alzheimer's disease and identifies extracellular matrix proteins as some of the earliest biomarkers of the disease. (nature.com)
  • Members of the European Platform for Neurodegenerative Diseases (EPND) announced today that they will embark on a venture to establish a collaborative platform for efficient sample and data sharing, leveraging and linking existing European research infrastructures to accelerate the discovery of biomarkers, new diagnostics and treatments for the benefit of people with neurodegenerative diseases such as Alzheimer's and Parkinson's. (kcl.ac.uk)
  • The development of effective treatments requires biomarkers for early detection of disease in individuals, for assessing treatment efficacy, and for patient stratification. (kcl.ac.uk)
  • Readout Health is a digital biomarker company focusing on the metabolic management of chronic diseases through novel breath biomarkers. (mybiosense.com)
  • The panel of fluid- and imaging-based biomarkers available for neurodegenerative disease research is growing and has the potential to close important gaps in research and the clinic. (bvsalud.org)
  • Various biomarkers feature nuanced differences in strengths, limitations, and biases that must be considered when investigating disease etiology and clinical utility. (bvsalud.org)
  • PURPOSE OF REVIEW Along with separate review articles covering fluid and imaging biomarkers in this issue of Alzheimer's Research and Therapy , we present the result of a discussion from the 2019 Biomarkers in Neurodegenerative Diseases course at the University College London . (bvsalud.org)
  • However, clinical trials have developed certain compounds that could potentially change the future of Alzheimer's disease treatments. (wikipedia.org)
  • Understanding how to detect these diseases early would be of great value to clinical practice. (sciencedaily.com)
  • The team carried out a review of clinical evidence on the effect of carotenoids (and particularly lutein and zeaxanthin) on age-related disease and disability, which clearly demonstrated broad prophylactic and palliative outcomes. (nutraingredients.com)
  • Owing to the financial, societal, and personal impact of these diseases, etiologies, prevention, and treatment have become the major focus of basic and clinical research. (hindawi.com)
  • In this study, we sought to understand the disease stages and therapeutic hypotheses studied in clinical trials conducted in neurodegenerative diseases to date. (nature.com)
  • Our goals were to characterize clinical trials across major neurodegenerative disease indications, identifying correlations and temporal trends, particularly with regards to disease stages and molecular targets of drugs. (nature.com)
  • The European Platform for Neurodegenerative Diseases (EPND) integrates existing initiatives to build, grow, and deliver a scalable and self-sustainable platform for storage and analysis of high-quality clinical samples and data collections. (kcl.ac.uk)
  • Despite robust research efforts to accelerate biomarker discovery, at this time there are few secure, accessible ways for clinical samples and data to be discovered and shared within the neurodegenerative disease research community. (kcl.ac.uk)
  • Thanks to funding from the Innovative Medicines Initiative (IMI), EPND will begin a five-year effort to establish a self-sustaining network that will support the discovery, harmonization, storage and analysis of high-quality clinical samples and data from neurodegenerative disease research. (kcl.ac.uk)
  • There are multiple examples of conditions in which risk for Alzheimer's is elevated and regional brain glucose hypometabolism is present before the clinical onset of the disease. (integrativepractitioner.com)
  • This group of diseases is also characterized by an insidious onset in which neuropathological changes develop years before clinical presentation. (aao.org)
  • Sadly, the clinical picture is often ambiguous until the disease is advanced and a significant amount of neuronal tissue has been irreversibly lost. (aao.org)
  • Two studies underway at the Clinical Research Unit at The Neuro will use a promising new smartphone application to track the development of symptoms in those with Parkinson's Disease and REM Sleep Behaviour Disorder. (mcgill.ca)
  • developing a strategic research agenda for neurodegenerative diseases encompassing basic, clinical and social research, and the latter also includes models of healthcare delivery. (neurodegenerationresearch.eu)
  • The University of California Irvine (UCI) School of Medicine, Department of Pathology & Laboratory Medicine invites applications from MD, MD-PhD, or equivalent board-certified neuropathologists to contribute to an active Alzheimer Disease and Related Dementias (ADRD) research and clinical community. (uci.edu)
  • BIOSENSE™ is available directly to consumers and clinics and is utilized in the clinical setting where fat burn and nutritional ketosis therapy is used to manage chronic disease. (mybiosense.com)
  • Objective To compare the general clinical conditions and oral alterations, and also evaluate the prosthesis, in subjects diagnosed with Alzheimer's disease (AD) or Parkinson's disease (PD), attended at two geriatric centers in the city of Fortaleza - Ceará. (bvsalud.org)
  • Age of onset and clinical manifestations may vary widely among patients with a given lysosomal storage disease, and significant phenotypic heterogeneity between family members carrying identical mutations has been reported. (medscape.com)
  • This has led to active clinical trials evaluating the safety and efficacy of intrathecal enzyme delivery in several lysosomal storage diseases (see www.ClinicalTrials.gov ). (medscape.com)
  • Targeting APOE may be a potential approach for diagnosis, risk assessment, prevention, and treatment of various neurodegenerative and cardiovascular diseases in humans. (dovepress.com)
  • 1 Excessive production of reactive oxygen species can lead to oxidative stress which is associated with inflammation and neurodegenerative disease. (bmglabtech.com)
  • These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well. (wikipedia.org)
  • Neurodegenerative disease is on the rise globally due to aging populations 1 , highlighting a need for effective therapeutic interventions. (nature.com)
  • Understanding the mutations in APOE, their structural properties, and their isoforms is important to determine its role in various diseases and to advance the development of therapeutic strategies. (dovepress.com)
  • Targeting curli production in the gut may represent a general therapeutic approach to prevent or slow down the progression of protein aggregation diseases. (hku.hk)
  • This represents strategic progress in our goal to support the research of therapeutic nutritional ketosis research in chronic disease management. (mybiosense.com)
  • We know that a ketogenic diet that reduces inflammation in the human body, and as such it is reducing that fundamental mechanism that underlies Alzheimer's and Parkinson's, and diabetes, and coronary artery disease and, really, across the board all the chronic degenerative conditions, said Perlmutter. (integrativepractitioner.com)
  • 7 Taub Institute for Alzheimer Disease and the Aging Brain and Department of Pathology and Cell Biology and Neurology, Columbia University Medical Center, New York, NY, USA. (nih.gov)
  • More recently, the team has shown, first in Parkinson's, how pathology spreads from cell-to-cell in neurodegenerative diseases. (upenn.edu)
  • Writing in Nutritional Neuroscience ​, they explain that the antioxidant and anti-inflammatory properties of lutein (L) and zeaxanthin (Z) help ameliorate characteristic co-morbidities associated with age-related neurodegenerative diseases, like oxidative and inflammatory stress. (nutraingredients.com)
  • The Consortium consists of the EBC membership , the Network of European funding for Neuroscience research (NEURON) , Joint Programme - Neurodegenerative Disease Research (JPND) and the Human Brain Project (HBP) . (neurodegenerationresearch.eu)
  • This is a 3-year project which is a coordination action in support of the implementation of Joint Programming to combat neurogegenerative diseases (JPND). (neurodegenerationresearch.eu)
  • The ultimate goal of the Joint Programme on Neurodegenerative Disease (JPND) is to accelerate progress in understanding the causes of these debilitating conditions, leading to not only early diagnosis, and the development of new treatments and prevention, but also the provision of more effective medical and social care to improve the quality of life for patients and care givers. (neurodegenerationresearch.eu)
  • Common neurodegenerative diseases include Alzheimer's disease and Parkinson's disease. (nature.com)
  • This Perspective proposes a tripartite model involving the amygdala, hippocampus and striatum as key structures underlying cognitive dysfunction in Parkinson disease. (nature.com)
  • Not only is α-synuclein found in Lewy bodies characteristic of Parkinson disease, but also m. (biomedcentral.com)
  • The absence of a positive correlation between the geographic distribution of Lyme disease and the distribution of deaths due to Alzheimer disease, ALS, MS, and Parkinson disease provides further evidence that Lyme disease is not associated with the development of these neurodegenerative conditions. (cdc.gov)
  • Researchers have critically evaluated these proposed biologic associations between Lyme disease and Alzheimer disease, ALS, MS, and Parkinson disease, but none have found evidence of an association ( 12 - 21 ). (cdc.gov)
  • We compared Lyme disease incidence rates in each state with death rates for Alzheimer disease, ALS, MS, and Parkinson disease. (cdc.gov)
  • Age-adjusted death rates of Alzheimer disease, ALS, MS, and Parkinson disease during the same time period were obtained from the CDC WONDER (Centers for Disease Control and Prevention Wide-ranging Online Data for Epidemiologic Research) database ( http://wonder.cdc.gov/WelcomeT.html ). (cdc.gov)
  • and G20, Parkinson disease. (cdc.gov)
  • Pourrions-nous détecter des maladies neurologiques évolutives comme la maladie de Parkinson avant que les symptômes ne soient apparents, ou détecter des changements dans la façon dont votre médicament gère vos symptômes d'heure en heure? (mcgill.ca)
  • Leading researchers from across Europe will gather today in Stockholm to develop a European-wide research strategy to tackle neurodegenerative diseases such as Alzheimer s and Parkinson s Disease. (neurodegenerationresearch.eu)
  • Parkinson`s disease. (bvsalud.org)
  • Thanks to this Joint Programme, the best European medical researchers will be working together and pooling resources to help the millions of people who suffer from Alzheimer s and other neurodenegerative diseases. (neurodegenerationresearch.eu)
  • By making research more efficient and avoiding duplication of work, the Joint Programme will increase the prospects of real progress in preventing and treating these diseases. (neurodegenerationresearch.eu)
  • Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies (like proteinopathy) and induced cell death. (wikipedia.org)
  • According to the latest study by Dr. Ronald Postuma from the Research Institute of the MUHC and Dr. Jacques Montplaisir from the Université de Montréal and the Hôpital du Sacré-Cœur de Montréal, 52.4 per cent of patients with REM sleep behaviour disorder develop a neurodegenerative disease within 12 years following their initial diagnosis. (sciencedaily.com)
  • This study was funded by the Canadian Institutes of Health Research (CIHR) and the Fonds de la recherche en santé du Québec (FRSQ). (sciencedaily.com)
  • In this webinar, Dr. Julien Flament of Molecular Imaging Research Center (MIRCen, CEA), Fontenay-aux-Roses, France, will present an introduction to the theoretical background of Chemical Exchange Saturation Transfer (CEST) imaging and its potential in neurodegenerative disease research. (news-medical.net)
  • The initial research program is focused on "targets that contribute to a disease phenotype that is believed to underlie neurodegenerative disease and is modifiable by small molecules in a phenotypic screen," BridGene said. (fiercebiotech.com)
  • Researchers pursue a comprehensive array of research activities that extend from basic science methods of test tubes and cell culture systems to those involving animal models of neurodegenerative diseases. (upenn.edu)
  • Through Project ALS, the Wasserman family saw an important opportunity to guide and directly impact neurodegenerative disease research. (projectals.org)
  • Together, Project ALS and the Wasserman family unpacked what it meant for a foundation to guide research funding, and Project ALS initiated a true partnership between the family and neurodegenerative disease investigators. (projectals.org)
  • Neurodegenerative and neurodevelopmental diseases constitute a major health burden, and in spite of several decades of intensive research, the molecular mechanisms underlying these diseases are still poorly understood, and effective drug treatments are generally lacking. (alzheimer-europe.org)
  • Research by Colin MacDiarmid and David Eide is exploring how a shortage of zinc can contribute to diseases. (neurosciencenews.com)
  • This research opens a new direction to develop preventative measures for neurodegenerative diseases by targeting bacterial curli production in the human gut. (hku.hk)
  • Initial work has begun to develop and implement a Strategic Research Agenda to address the medical and societal impacts of neurodegenerative diseases. (neurodegenerationresearch.eu)
  • By doing this we will optimise research investment in neurodegenerative disease across Europe. (neurodegenerationresearch.eu)
  • A Scientific Advisory Board comprising 15 of the top neurodegenerative disease scientists from Europe and elsewhere in the world has been formed to advise on the development of the Strategic Research Agenda and its implementation. (neurodegenerationresearch.eu)
  • A recent research on a genetic heart disease has uncovered a new and unexpected mechanism for heart failure. (devdiscourse.com)
  • Considering the varied strengths, limitations, and biases of different research methodologies and approaches may help harmonize disciplines within the neurodegenerative disease field. (bvsalud.org)
  • Lastly, we highlight novel modalities that have been proposed in the landscape of neurodegenerative disease research and care. (bvsalud.org)
  • Alzheimer's disease (AD) is a chronic neurodegenerative disease that results in the loss of neurons and synapses in the cerebral cortex and certain subcortical structures, resulting in gross atrophy of the temporal lobe, parietal lobe, and parts of the frontal cortex and cingulate gyrus. (wikipedia.org)
  • Alzheimer's disease is a complex and chronic disease that evolves over decades. (nature.com)
  • Alzheimer's disease is the sixth leading cause of death among U.S. adults, yet the chronic neurodegenerative disease has no cure or effective treatment. (scienceblog.com)
  • however, a variable but measurable amount of AD pathologic changes exist in most cognitively intact elderly individuals who undergo autopsy, indicating that AD is a chronic disease with latent and prodromal stages and suggesting that individuals may have varying abilities to compensate, either biologically or functionally, for the presence of AD. (medscape.com)
  • With the Project ALS Therapeutics Core team, Dr. Chavez is developing a unique system in which drugs can be tested against multiple genetic mutations causing ALS, and even other neurodegenerative diseases like Alzheimer's and Parkinson's, in one screen. (projectals.org)
  • To date, the group has introduced 217 genetic mutations known to cause ALS, Parkinson's, Alzheimer's, and other neurodegenerative diseases into a single system, and with The Bert and Sandra Wasserman Foundation's support, they are now poised to test thousands of potential drugs on this comprehensive model of fatal brain diseases. (projectals.org)
  • Several point mutations in the KIF1A motor domain have been identified in patients with various motor neuron diseases. (biorxiv.org)
  • Our study provides the first comprehensive demonstration of KIF1A disease mutations at the molecular level. (biorxiv.org)
  • In addition, mutations in mitochondrial DNA have been associated with an increased risk of the disease. (bmglabtech.com)
  • Mutations in the PINK1 gene (also known as PARK6) are associated with early onset Parkinson's disease. (bmglabtech.com)
  • This presentation explored EVs and their role in neurogenerative diseases, with a particular focus on prion diseases. (izon.com)
  • The accumulation of protein misfolding is a common hallmark of neurodegenerative diseases, and prion diseases are no exception. (izon.com)
  • Prion diseases are characterised by the presence of abnormal, pathogenic agents that can induce abnormal folding of specific normal cellular proteins called prion proteins. (izon.com)
  • The identification of prion propagation mechanisms is an important aspect of understanding prion diseases, as PRPsc (the disease-associated conformation) can trigger healthy prion proteins (PRP) to fold abnormally. (izon.com)
  • As the normal form of the prion protein is susceptible to digestion by protease K, western blots could be used to distinguish between normal and disease-associated forms of the protein. (izon.com)
  • Evidence supporting a role for EVs in propagating the spread of disease-associated prion proteins has been drawn from a number of studies highlighted during the presentation. (izon.com)
  • For example, prion disease can be induced in mice by administering EVs isolated from injected fibroblast and neuronal cell lines. (izon.com)
  • have been identified in ALS and related motor neuron diseases. (frontiersin.org)
  • It is thought that defects in protein transport machinery and regulation, such as RAB1, may play a role in this disease mechanism. (wikipedia.org)
  • We aim to gain novel insights into the molecular mechanisms underlying these diseases, with a particular focus on defects in protein synthesis. (alzheimer-europe.org)
  • By combining the complementary technical and thematic expertise of the consortium partners, we expect to gain unprecedented insights into the molecular mechanisms of these diseases and their associated defects in protein synthesis. (alzheimer-europe.org)
  • Neurodegenerative diseases are caused by protein aggregation in the neurons. (hku.hk)
  • CTE is a neurodegenerative brain disease initiated by repeated head traumas, which cause a buildup of tau protein in blood vessels. (dailyfreepress.com)
  • The medication being tested in the PADOVA trial aims to reduce the level of a protein involved in the development of Parkinson's Disease and to stop its spread from cell to cell. (mcgill.ca)
  • This landmark discovery found a correlation between the clumping of RNA-binding proteins long linked to neurodegenerative disease and the aggregates of protein found in the heart tissue of patients with RBM20 dilated cardiomyopathy. (devdiscourse.com)
  • To my knowledge, this overload of protein granules in cells has only previously been seen in the brain or spinal cord, and some very rare skeletal muscle diseases. (devdiscourse.com)
  • What have worm models told us about the mechanisms of neuronal dysfunction in human neurodegenerative diseases? (biomedcentral.com)
  • Are common mechanisms at play in different diseases? (alzheimer-europe.org)
  • Genetically modified animals are invaluable models to understand the molecular disease mechanisms and to screen for modifying compounds. (karger.com)
  • A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. (wikipedia.org)
  • Experiments have revealed reduced transport rates of both wild-type and two familial Parkinson's disease-associated mutant alpha-synucleins through axons of cultured neurons. (wikipedia.org)
  • What kills neurons in neurodegenerative disease? (biomedcentral.com)
  • Alzheimer's disease causes neurons and synapses in the brain to deteriorate deteriorate slowly and irreversibly. (scienceblog.com)
  • Because the herpesvirus sits in neurons forever, there is speculation it is connected to neurodegenerative diseases. (scitechdaily.com)
  • Although effective treatments against REM sleep behaviour disorder do exist, these medications do not postpone the onset of neurodegenerative disease. (sciencedaily.com)
  • By combining chemoproteomics and covalent small molecules, BridGene will try to identify the targets responsible for the onset and progression of disease and show which targets a drug candidate interacts with in live cells. (fiercebiotech.com)
  • In ALS alone, more than 50 genes have been implicated in disease onset. (projectals.org)
  • Preventative medicine should start at the top, well before onset of neurodegenerative disease. (integrativepractitioner.com)
  • The presence of oligogenic variants did not influence the age of onset or disease severity. (bmj.com)
  • Alzheimer s disease is particularly expensive to manage due to its insidious onset, its ever-increasing levels of disability and the length of time over which the condition extends itself. (neurodegenerationresearch.eu)
  • Enzyme replacement therapy (ERT) appears safe and effective for peripheral manifestations in patients with Gaucher disease types I and III, Fabry disease, mucopolysaccharidosis I (Hurler, Hurler-Scheie, and Scheie syndromes), mucopolysaccharidosis II (Hunter syndrome), mucopolysaccharidosis VI (Maroteaux-Lamy syndrome), Pompe disease, and recently Batten disease (neuronal ceroid lipofuscinoses, CLN2). (medscape.com)
  • Despite this, the genetic basis of the disorder is not well defined and its boundaries with other neurodegenerative diseases are unclear. (nih.gov)
  • Although women generally live longer than men, they are much more likely to suffer from age-related disease and disability, which US researchers believe could be prevented through lifestyle changes. (nutraingredients.com)
  • Researchers maintain increased intake has the potential to reduce visual and cognitive dysfunction and inhibit neurodegenerative disease progression. (nutraingredients.com)
  • Researchers provide the example of a 90-year-old female with amyloid plaques having a lifetime risk of Alzheimer's disease of only 8.4 percent, compared to a 65-year-old female with amyloid plaques who has a lifetime risk of 29.3 percent. (neurodegenerationresearch.eu)
  • Here, we performed whole exome sequencing of a cohort of 1118 Caucasian DLB patients, and focused on genes causative of monogenic neurodegenerative diseases. (nih.gov)
  • We will use mouse models for the respective diseases, and apply a novel methodology to identify and quantify proteins and their levels in specific cell types in these mouse models. (alzheimer-europe.org)
  • Scientists at UW-Madison have made a discovery that, if replicated in humans, suggests a shortage of zinc may contribute to diseases like Alzheimer's and Parkinson's, which have been linked to defective proteins clumping together in the brain. (neurosciencenews.com)
  • If low zinc supply has the same effect on human cells as on yeast, zinc deficiency might contribute to human diseases that are associated with a build-up of "junked" proteins, such as Parkinson's and Alzheimer's. (neurosciencenews.com)
  • Inhibiting the ability of the bacteria to secrete such proteins may be a preventative treatment for neurodegenerative diseases. (hku.hk)
  • Extracellular vesicles (EVs) play a key role in propagating the spread of disease-related proteins in neurodegenerative diseases - that was one of the key messages delivered during ISEV2021's first plenary session by Andrew Hill of La Trobe University , Australia. (izon.com)
  • Recent advances in neuroimaging methods have revealed that pathological proteins accumulate along specific macroscale brain networks, implicating the network architecture of the brain in the system-level pathophysiology of neurodegenerative diseases. (lu.se)
  • More recently, the concept of lysosomal storage disease has been expanded to include deficiencies or defects in proteins necessary for the normal post-translational modification of lysosomal enzymes (which themselves are often glycoproteins), activator proteins, or proteins important for proper intracellular trafficking between the lysosome and other intracellular compartments. (medscape.com)
  • In this blog, we look at the relationship between mitochondrial dysfunction and neurodegenerative disease. (bmglabtech.com)
  • Several lines of evidence suggest the involvement of mitochondrial dysfunction in Alzheimer's disease. (bmglabtech.com)
  • Evidence also points to multiple genes being linked to mitochondrial dysfunction in Alzheimer's disease. (bmglabtech.com)
  • Altered mitochondrial dynamics, including excessive fission and fusion of mitochondria, also contribute to mitochondrial dysfunction in Alzheimer's disease. (bmglabtech.com)
  • In Parkinson's disease, a strong link between mitochondrial dysfunction and disease-associated genes has been documented. (bmglabtech.com)
  • However, the new discovery finds another way that mutant RBM20 damages heart muscle cells: through accumulation of pathological ribonucleoprotein granules, affecting everything in the cells and leading to a new form of disease. (devdiscourse.com)
  • 2019). Elevated concentrations of NfL have also been associated with disease severity in these patient populations, including in MS and other neurologic conditions (Disanto et al. (cdc.gov)
  • The study showed that the chance a patient suffering from an REM sleep behaviour disorder will develop a neurodegenerative disease is 17.7 per cent within five years of diagnosis, 40.6 per cent within 10 years, and 52.4 per cent within 12 years. (sciencedaily.com)
  • When I spoke to my husband's Parkinson's doctor fifteen years after his diagnosis, he told me there had not been one change in treatment or knowledge of the disease. (projectals.org)
  • Parkinson's disease (PD) is the second most common neurodegenerative disorder. (wikipedia.org)
  • Membrane damage by alpha-synuclein could be another Parkinson's disease mechanism. (wikipedia.org)
  • Problems with the sense of smell is a widespread symptom of Parkinson's disease (PD), however, some neurologists question its efficacy. (wikipedia.org)
  • Parkinson's disease (PD) "off"-period symptoms control is better following administration of an inhaled levodopa powder formulation (CVT-301) than placebo. (empr.com)
  • Patients with advanced Parkinson's disease had resting tremors improved with levodopa-carbidopa intestinal gel, a study presented at the 68th Annual AAN Meeting has found. (empr.com)
  • We are entering a new age of monitoring in Parkinson's Disease," explains Dr. Postuma. (mcgill.ca)
  • This observational study will look at individuals diagnosed with Parkinson's Disease, REM Sleep Behaviour Disorder as well as healthy participants. (mcgill.ca)
  • The application will allow us to design more sensitive trials for Parkinson's disease and to be better able to test new medication," adds Dr. Postuma. (mcgill.ca)
  • Even with billions of dollars being used to find a treatment for Alzheimer's disease, no effective treatments have been found. (wikipedia.org)
  • The authors present the results of a phase 2 study of gosuranemab, a monoclonal antibody targeting N-terminal tau, in patients with early Alzheimer's disease. (nature.com)
  • For patients with moderate to severe Alzheimer's disease, adding memantine to cholinesterase inhibitor treatment can improve daily life task functions, results of post-hoc pooled factor analysis presented at the 68th AAN Annual Meeting have shown. (empr.com)
  • Founded in 1991, CNDR became the first and only National Institutes of Health (NIH)-funded Alzheimer's Disease Core Center (ADCC) in the Delaware Valley, part of a network of several cooperating NIH-funded centers throughout the nation. (upenn.edu)
  • More than 20 years ago, the team identified the significance of tau in Alzheimer's disease, later identifying TDP-43's role in other neurodegenerative diseases. (upenn.edu)
  • Now in her eighties, Sandra has friends experiencing the debilitating consequences of Alzheimer's disease and has seen what each of these diseases can do to a person's physicality, mental wellness, and to relationships within families. (projectals.org)
  • The pharmaceutical industry is losing its battle in terms of developing a magic bullet for Alzheimer's disease. (integrativepractitioner.com)
  • There are multiple reasons why the ketogenic diet is an ideal preventative approach to Alzheimer's disease and other age-related diseases. (integrativepractitioner.com)
  • The disruption of mitochondrial function is a known contributor to neurodegenerative diseases like Parkinson's and Alzheimer's disease, although the precise details remain to be worked out. (bmglabtech.com)
  • In addition to less ATP production and higher levels of reactive oxygen species, mitochondria in the brains of individuals with Alzheimer's disease show mitochondrial abnormalities that include altered shape, decreased density, and impaired respiration. (bmglabtech.com)
  • In this context, studies using positron emission tomography have indicated decreased use of glucose and impaired oxidative metabolism in the brains of patients with Alzheimer's disease. (bmglabtech.com)
  • Alzheimer's disease (AD) is the most common NDD, affecting an estimated 5 million Americans. (aao.org)
  • Beta-amyloid deposits (plaques) are found in the brains of patients with Alzheimer's disease. (brainfoundation.org.au)
  • This study will also look at memory performance, brain grey matter volume, and other factors known to increase risk of Alzheimer's disease and see how they interact with OSA and amyloid plaque burden. (brainfoundation.org.au)
  • Use of a panel of 16 differentially expressed EV-miRNAs to 'predict' Alzheimer's disease (AD) in serum samples of healthy individuals and in people who had been diagnosed with AD. (izon.com)
  • These early changes are referred to as preclinical Alzheimer's disease. (neurodegenerationresearch.eu)
  • EMFs and Alzheimer's disease (letter). (cdc.gov)
  • Existing treatments for neurodegenerative diseases are limited, and mainly treat the symptoms, rather than addressing the cause. (neurodegenerationresearch.eu)
  • The authors conclude that this study indicates that neurodegenerative diseases occur more frequently in some occupations than in others. (cdc.gov)
  • While PD is the second most common neurodegenerative disorder, problems with diagnoses still persist. (wikipedia.org)
  • REM sleep behavior disorder appears to be a predictor of neurodegenerative disease in more than 50 percent of cases. (sciencedaily.com)
  • Department of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK. (bvsalud.org)
  • however, an inverse correlation was detected between Lyme disease and Alzheimer disease. (cdc.gov)
  • Neurodegenerative disease will be the first area to benefit from this new approach, with particular emphasis on Alzheimer s disease. (neurodegenerationresearch.eu)
  • However, knowledge about how these vaccines work, how the immune system works and how neurodegenerative diseases come about can be brought to bear on the problem in order to predict potential devastating future consequences of the vaccines. (theepochtimes.com)
  • These studies summarize Perlmutter's idea that age-related disease prevention should start as early as possible. (integrativepractitioner.com)
  • Centers for Disease Control and Prevention. (cdc.gov)
  • The Centers for Disease Control and Prevention (CDC) cannot attest to the accuracy of a non-federal website. (cdc.gov)