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)
A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.
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.
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)
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
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.
Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.
Neurons whose primary neurotransmitter is DOPAMINE.
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.
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.
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.
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 family of peptidyl-prolyl cis-trans isomerases that bind to CYCLOSPORINS and regulate the IMMUNE SYSTEM. EC 5.2.1.-
A sporadic neurodegenerative disease with onset in middle-age characterized clinically by Parkinsonian features (e.g., MUSCLE RIGIDITY; HYPOKINESIA; stooped posture) and HYPOTENSION. This condition is considered a clinical variant of MULTIPLE SYSTEM ATROPHY. Pathologic features include a prominent loss of neurons in the zona compacta of the SUBSTANTIA NIGRA and PUTAMEN. (From Adams et al., Principles of Neurology, 6th ed, p1075-6)
A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.
An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4.
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 deaminated metabolite of LEVODOPA.
Homovanillic acid (HVA) is a major metabolite of dopamine, formed in the body through the catabolic breakdown of this neurotransmitter by the enzyme catechol-O-methyltransferase and then further metabolized in the liver before excretion in urine.
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.
The phylogenetically newer part of the CORPUS STRIATUM consisting of the CAUDATE NUCLEUS and PUTAMEN. It is often called simply the striatum.
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.
Agents used in the treatment of Parkinson's disease. The most commonly used drugs act on the dopaminergic system in the striatum and basal ganglia or are centrally acting muscarinic antagonists.
The mitochondria of the myocardium.
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.
A chemically heterogeneous group of drugs that have in common the ability to block oxidative deamination of naturally occurring monoamines. (From Gilman, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p414)
Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of dopaminergic neurons. They remove DOPAMINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS and are the target of DOPAMINE UPTAKE INHIBITORS.
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.
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 cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).
The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.
Tricyclic anorexigenic agent unrelated to and less toxic than AMPHETAMINE, but with some similar side effects. It inhibits uptake of catecholamines and blocks the binding of cocaine to the dopamine uptake transporter.
A genus of the subfamily CALLITRICHINAE occurring in forests of Brazil and Bolivia and containing seventeen species.
The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.
Pyridinium compounds are organic salts formed when pyridine, a basic heterocyclic organic compound, reacts with acids, resulting in a positively charged nitrogen atom surrounded by aromatic rings.
Manganese derivative of ethylenebisdithiocarbamate. It is used in agriculture as a fungicide and has been shown to cause irritation to the eyes, nose, skin, and throat.
Manganese poisoning is associated with chronic inhalation of manganese particles by individuals who work with manganese ore. Clinical features include CONFUSION; HALLUCINATIONS; and an extrapyramidal syndrome (PARKINSON DISEASE, SECONDARY) that includes rigidity; DYSTONIA; retropulsion; and TREMOR. (Adams, Principles of Neurology, 6th ed, p1213)
An agricultural fungicide of the dithiocarbamate class. It has relatively low toxicity and there is little evidence of human injury from exposure.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A trace element with atomic symbol Mn, atomic number 25, and atomic weight 54.94. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver. (From AMA Drug Evaluations Annual 1992, p2035)
The passive movement of molecules exceeding the rate expected by simple diffusion. No energy is expended in the process. It is achieved by the introduction of passively diffusing molecules to an enviroment or path that is more favorable to the movement of those molecules. Examples of facilitated diffusion are passive transport of hydrophilic substances across a lipid membrane through hydrophilic pores that traverse the membrane, and the sliding of a DNA BINDING PROTEIN along a strand of DNA.
Abnormal involuntary movements which primarily affect the extremities, trunk, or jaw that occur as a manifestation of an underlying disease process. Conditions which feature recurrent or persistent episodes of dyskinesia as a primary manifestation of disease may be referred to as dyskinesia syndromes (see MOVEMENT DISORDERS). Dyskinesias are also a relatively common manifestation of BASAL GANGLIA DISEASES.

Recovery of chronic parkinsonian monkeys by autotransplants of carotid body cell aggregates into putamen. (1/246)

We have studied the effect of unilateral autografts of carotid body cell aggregates into the putamen of MPTP-treated monkeys with chronic parkinsonism. Two to four weeks after transplantation, the monkeys initiated a progressive recovery of mobility with reduction of tremor and bradykinesia and restoration of fine motor abilities on the contralateral side. Apomorphine injections induced rotations toward the side of the transplant. Functional recovery was accompanied by the survival of tyrosine hydroxylase-positive (TH-positive) grafted glomus cells. A high density of TH-immunoreactive fibers was seen reinnervating broad regions of the ipsilateral putamen and caudate nucleus. The nongrafted, contralateral striatum remained deafferented. Intrastriatal autografting of carotid body tissue is a feasible technique with beneficial effects on parkinsonian monkeys; thus, this therapeutic approach could also be applied to treat patients with Parkinson's disease.  (+info)

Regional and temporal expression of the peripheral benzodiazepine receptor in MPTP neurotoxicity. (2/246)

We used the dopaminergic neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to evaluate the sensitivity and specificity of the peripheral benzodiazepine receptor (PBR) as a biomarker of chemical-induced neurotoxicity. Receptor autoradiography of [3H]-PK11195, a PBR selective ligand, indicated dose-dependent increases throughout the nigrostriatal dopaminergic system as early as 24 h after MPTP administration (10-80 mg/kg), which persisted for at least 21 days. The binding of [3H]-PK11195 was increased as much as 98% in the corpus striatum and 114% in the substantia nigra, following MPTP exposure. The integrity of nigrostriatal dopaminergic terminals in the corpus striatum was assessed by measuring high affinity dopamine transporter (DAT) levels and dopamine content. DAT levels were measured by [3H]-WIN 35,428 autoradiography, and dopamine content decreased with increasing MPTP dose. Reductions of both indices of dopaminergic terminal integrity correlated with increased levels of [3H]-PK11195-binding in the striatum (r2 = 0.84 for DAT and 0.93 for dopamine content). Tyrosine hydroxylase (TH) immunohistochemistry demonstrated dose-dependent reductions of dopaminergic neurons in the substantia nigra pars compacta, with a 67% loss measured 7 days after treatment with 80 mg/kg MPTP. The loss of TH-positive neurons was correlated (r2 = 0.95) with increased levels of [3H]-PK11195 binding in the substantia nigra. These findings demonstrate that the PBR is both sensitive and specific for identifying brain regions involved in MPTP neurotoxicity.  (+info)

Differing effects of N-methyl-D-aspartate receptor subtype selective antagonists on dyskinesias in levodopa-treated 1-methyl-4-phenyl-tetrahydropyridine monkeys. (3/246)

The antiparkinsonian and antidyskinetic profile of two N-methyl-D-aspartate (NMDA) receptor antagonists, a competitive antagonist, (R)-4-oxo-5-phosphononorvaline (MDL 100,453), and a novel noncompetitive allosteric site antagonist, 4-hydroxy-N-[2-(4-hydroxyphenoxy)ethyl]-4-(4-methylbenzyl)piper idi ne (Co 101244/PD 174494), was assessed in six levodopa-treated 1-methyl-4-phenyl-tetrahydropyridine-lesioned parkinsonian monkeys. The effects on motor function of these two drugs, alone and in combination with levodopa, were then correlated with NMDA subtype selectivity and apparent affinity for four diheteromeric NMDA receptor subunit combinations expressed in Xenopus oocytes. MDL 100, 453 (300 mg/kg s.c.) by itself increased global motor activity (p =. 0005 versus vehicle) and administered 15 min after a low dose of levodopa/benserazide s.c., MDL 100,453 (50, 300 mg/kg s.c.) showed dose-dependent potentiation of antiparkinsonian responses and also produced dyskinesias. Following injection of a fully effective dose of levodopa, MDL 100,453 (300 mg/kg s.c.) also produced a 25% increase in mean dyskinesia score (p =.04). In contrast, Co 101244 did not change motor activity by itself and only showed a tendency to potentiate the antiparkinsonian response when given in combination with a low dose of levodopa, which did not attain statistical significance. However, with a high dose of levodopa, Co 101244 (0.1, 1 mg/kg s.c.) displayed antidyskinetic effects (67 and 71% reduction, respectively) while sparing levodopa motor benefit. In vitro, MDL 100,453 was an NMDA glutamate-site antagonist, with approximately 5- to 10-fold selectivity for the NR1A/NR2A subtype combination (K(b) = 0.6 microM) versus NR1A in combination with 2B, 2C, or 2D. In contrast, the allosteric site antagonist Co 101244 showed approximately 10,000-fold selectivity for the NR1A/NR2B (IC(50) = 0.026 microM) versus the other three subunit combinations tested. Taken together, the data suggest that the NR2 subunit selectivity profile of NMDA receptor antagonists can play an important role in predicting behavioral outcome and offer more evidence that NR2B-selective NMDA receptor antagonists may be useful agents in the treatment of Parkinson's disease.  (+info)

Mice deficient in cellular glutathione peroxidase show increased vulnerability to malonate, 3-nitropropionic acid, and 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine. (4/246)

Glutathione peroxidase (GSHPx) is a critical intracellular enzyme involved in detoxification of hydrogen peroxide (H(2)O(2)) to water. In the present study we examined the susceptibility of mice with a disruption of the glutathione peroxidase gene to the neurotoxic effects of malonate, 3-nitropropionic acid (3-NP), and 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). Glutathione peroxidase knock-out mice showed no evidence of neuropathological or behavioral abnormalities at 2-3 months of age. Intrastriatal injections of malonate resulted in a significant twofold increase in lesion volume in homozygote GSHPx knock-out mice as compared to both heterozygote GSHPx knock-out and wild-type control mice. Malonate-induced increases in conversion of salicylate to 2,3- and 2, 5-dihydroxybenzoic acid, an index of hydroxyl radical generation, were greater in homozygote GSHPx knock-out mice as compared with both heterozygote GSHPx knock-out and wild-type control mice. Administration of MPTP resulted in significantly greater depletions of dopamine, 3,4-dihydroxybenzoic acid, and homovanillic acid in GSHPx knock-out mice than those seen in wild-type control mice. Striatal 3-nitrotyrosine (3-NT) concentrations after MPTP were significantly increased in GSHPx knock-out mice as compared with wild-type control mice. Systemic 3-NP administration resulted in significantly greater striatal damage and increases in 3-NT in GSHPx knock-out mice as compared to wild-type control mice. The present results indicate that a knock-out of GSHPx may be adequately compensated under nonstressed conditions, but that after administration of mitochondrial toxins GSHPx plays an important role in detoxifying increases in oxygen radicals.  (+info)

Ratio of inhibited-to-activated pallidal neurons decreases dramatically during passive limb movement in the MPTP-treated monkey. (5/246)

Mink advanced the hypothesis in 1996 that the role of the basal ganglia (BG) is primarily one of focused selection; the encouragement of motor mechanisms inducing a desired movement and the inhibition of competing mechanisms. This would imply, in normal subjects, a ratio of inhibited-to-activated (I/A) movement-related globus pallidus pars internalis (GPi) neurons <1 and a drastic decrease of this ratio in the parkinsonian state. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication should therefore decrease the specificity of the response of this neuronal population. To test this working hypothesis we studied the activity of GPi neurons in response to passive limb movement in the normal and the parkinsonian monkey. Extracellular unit recordings monitored any correlation between passive limb movements and eventual modifications of the neuronal activity of the GPi in two calm, awake, and drug naive monkeys (Macaca fascicularis) before and after MPTP intoxication. In the normal animal, arm- and leg-related neurons were located in clusters in the medial part of the GPi. The I/A ratio was 0.22. Most GPi cells were linked to a single joint. In the MPTP-treated monkey, the number of movement-related neurons increased, the I/A ratio dropped significantly to 0.03, and most responding cells were linked to several joints. These data, which cannot be explained by the classic "box" model, endorse Mink's hypothesis.  (+info)

The VMAT2 gene in mice and humans: amphetamine responses, locomotion, cardiac arrhythmias, aging, and vulnerability to dopaminergic toxins. (6/246)

Monoamine compartmentalization in monoaminergic neurons uses serial action of the plasma membrane and vesicular monoamine (VAMT2) transporters. We can now define the sequences of the genes encoding these transporters in mice and humans, examine influences of deletions of this gene and alteration in its expression levels in transgenic mice, and identify sequence polymorphisms in the human VMAT2 gene. Examination of VMAT2 variants can provide potential insights into roles for allelic variants at these loci in variant drug responses and in diseases linked to monoaminergic systems, including substance abuse and Parkinson's disease.  (+info)

Structural MRI as a tool for the study of neurotoxicity and neurodegenerative disorders. (7/246)

High-resolution magnetic resonance (MR) imaging affords an unprecedented opportunity to study the severity and distribution of neurodegenerative changes in the human brain. By selecting specific MR sequence parameters (i.e., TE and TR), different MR signals can be received from different tissue types, such as gray and white matter. Through optimization of the contrast between different tissue types, the surfaces and internal structures of brain structures of special interest can be visualized and quantitated. Metrics such as two-dimensional areas, three-dimensional volumes, and three-dimensional shape characteristics have proven to be highly useful for quantitating the effects of toxins on the human brain. Among toxins, the effects of alcohol on the human brain have been most intensively studied using structural MR imaging. Volume losses in the cerebral cortex and other brain regions of interest have been carefully quantitated. However, because exposure to alcohol is almost always repeated over many years, the effects of normal aging must be carefully considered when making comparisons between diseased and healthy populations. In contrast to the literature on alcohol, structural MR imaging has been relatively underutilized in the study of drugs and other chemicals such as MPTP and other drugs of abuse that are toxic to special populations of neurons. However, as the resolution of structural MR continues to improve, the structural characteristics of such neuron populations will be visualized and quantitated, and successful use of structural MR imaging for the study of such toxins will become possible.  (+info)

Gene transfer of the JNK interacting protein-1 protects dopaminergic neurons in the MPTP model of Parkinson's disease. (8/246)

Increasing evidence suggests that apoptosis may be the underlying cell death mechanism in the selective loss of dopaminergic neurons in Parkinson's disease. Because the inhibition of caspases provides only partial protection in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/1-methyl-4-phenylpyridinium (MPTP/MPP(+)) model of Parkinson's disease, we investigated the role of the proapoptotic c-Jun N-terminal kinase (JNK) signaling cascade in SH-SY5Y human neuroblastoma cells in vitro and in mice in vivo. MPTP/MPP(+) led to the sequential phosphorylation and activation of JNK kinase (MKK4), JNK, and c-Jun, the activation of caspases, and apoptosis. In mice, adenoviral gene transfer of the JNK binding domain of JNK-interacting protein-1 (a scaffold protein and inhibitor of JNK) inhibited this cascade downstream of MKK4 phosphorylation, blocked JNK, c-Jun, and caspase activation, the death of dopaminergic neurons, and the loss of catecholamines in the striatum. Furthermore, the gene transfer resulted in behavioral benefit. Therefore, inhibition of the JNK pathway offers a new treatment strategy for Parkinson's disease that blocks the death signaling pathway upstream of the execution of apoptosis in dopaminergic neurons, providing a therapeutic advantage over the direct inhibition of caspases.  (+info)

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.

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.

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.

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.

Mitochondrial membrane transport proteins are a type of integral membrane proteins located in the inner and outer mitochondrial membranes. They play a crucial role in the regulation of molecule exchange between the cytosol and the mitochondrial matrix, allowing only specific ions and molecules to pass through while maintaining the structural and functional integrity of the mitochondria.

The inner mitochondrial membrane transport proteins, also known as the mitochondrial carrier proteins or the solute carriers, are a family of about 50 different types of proteins that facilitate the passage of various metabolites, such as nucleotides, amino acids, fatty acids, and inorganic ions (like calcium, sodium, and potassium). These transport proteins usually function as exchangers or uniporters, moving one type of solute in one direction in exchange for another type of solute or a proton.

The outer mitochondrial membrane is more permeable than the inner membrane due to the presence of voltage-dependent anion channels (VDACs) and other porins that allow small molecules, ions, and metabolites to pass through. VDACs are the most abundant proteins in the outer mitochondrial membrane and play a significant role in controlling the flow of metabolites between the cytosol and the intermembrane space.

In summary, mitochondrial membrane transport proteins are essential for maintaining the proper functioning of mitochondria by regulating the movement of molecules across the inner and outer membranes. They facilitate the exchange of nutrients, metabolites, and ions required for oxidative phosphorylation, energy production, and other cellular processes.

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.

Dopamine agents are medications that act on dopamine receptors in the brain. Dopamine is a neurotransmitter, a chemical messenger that transmits signals in the brain and other areas of the body. It plays important roles in many functions, including movement, motivation, emotion, and cognition.

Dopamine agents can be classified into several categories based on their mechanism of action:

1. Dopamine agonists: These medications bind to dopamine receptors and mimic the effects of dopamine. They are used to treat conditions such as Parkinson's disease, restless legs syndrome, and certain types of dopamine-responsive dystonia. Examples include pramipexole, ropinirole, and rotigotine.
2. Dopamine precursors: These medications provide the building blocks for the body to produce dopamine. Levodopa is a commonly used dopamine precursor that is converted to dopamine in the brain. It is often used in combination with carbidopa, which helps to prevent levodopa from being broken down before it reaches the brain.
3. Dopamine antagonists: These medications block the action of dopamine at its receptors. They are used to treat conditions such as schizophrenia and certain types of nausea and vomiting. Examples include haloperidol, risperidone, and metoclopramide.
4. Dopamine reuptake inhibitors: These medications increase the amount of dopamine available in the synapse (the space between two neurons) by preventing its reuptake into the presynaptic neuron. They are used to treat conditions such as attention deficit hyperactivity disorder (ADHD) and depression. Examples include bupropion and nomifensine.
5. Dopamine release inhibitors: These medications prevent the release of dopamine from presynaptic neurons. They are used to treat conditions such as Tourette's syndrome and certain types of chronic pain. Examples include tetrabenazine and deutetrabenazine.

It is important to note that dopamine agents can have significant side effects, including addiction, movement disorders, and psychiatric symptoms. Therefore, they should be used under the close supervision of a healthcare provider.

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.

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.

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.

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.

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.

Cyclophilins are a family of proteins that have peptidyl-prolyl isomerase activity, which means they help with the folding and functioning of other proteins in cells. They were first identified as binding proteins for the immunosuppressive drug cyclosporine A, hence their name.

Cyclophilins are found in various organisms, including humans, and play important roles in many cellular processes such as signal transduction, protein trafficking, and gene expression. In addition to their role in normal cell function, cyclophilins have also been implicated in several diseases, including viral infections, cancer, and neurodegenerative disorders.

In medicine, the most well-known use of cyclophilins is as a target for immunosuppressive drugs used in organ transplantation. Cyclosporine A and its derivatives work by binding to cyclophilins, which inhibits their activity and subsequently suppresses the immune response.

Striatonigral degeneration (SND) is a type of neurodegenerative disorder that affects the basal ganglia, specifically the striatum and the substantia nigra. It is also known as "striatonigral degeneration with olivopontocerebellar atrophy" or "multiple system atrophy-parkinsonian type (MSA-P)".

SND is characterized by the progressive loss of nerve cells in the striatum, which receives input from the cerebral cortex and sends output to the substantia nigra. This results in a decrease in the neurotransmitter dopamine, leading to symptoms similar to those seen in Parkinson's disease (PD), such as stiffness, slowness of movement, rigidity, and tremors.

However, unlike PD, SND is also associated with degeneration of the olivopontocerebellar system, which can lead to additional symptoms such as ataxia, dysarthria, and oculomotor abnormalities. The exact cause of striatonigral degeneration is unknown, but it is believed to involve a combination of genetic and environmental factors. Currently, there is no cure for the condition, and treatment is focused on managing the symptoms.

Selegiline is a selective, irreversible MAO-B inhibitor, which is primarily used in the clinical management of Parkinson's disease. It works by blocking the action of monoamine oxidase B (MAO-B), an enzyme responsible for breaking down dopamine, a neurotransmitter involved in movement regulation. By inhibiting MAO-B, selegiline increases the availability of dopamine in the brain, thereby helping to alleviate symptoms of Parkinson's disease such as stiffness, tremors, and spasms.

Selegiline is also available under the brand name Eldepryl, Zelapar, and Emsam. In addition to its use in Parkinson's disease, selegiline has been explored for its potential benefits in treating depression, dementia, and other neurological disorders. However, its use in these conditions is still considered off-label and requires careful consideration of the potential risks and benefits.

It is important to note that MAO inhibitors like selegiline can have serious interactions with certain foods and medications, particularly those containing tyramine, which can lead to a dangerous increase in blood pressure (hypertensive crisis). Therefore, it is crucial to follow strict dietary restrictions and medication guidelines when taking selegiline or any other MAO inhibitor.

Monoamine oxidase (MAO) is an enzyme found on the outer membrane of mitochondria in cells throughout the body, but primarily in the gastrointestinal tract, liver, and central nervous system. It plays a crucial role in the metabolism of neurotransmitters and dietary amines by catalyzing the oxidative deamination of monoamines. This enzyme exists in two forms: MAO-A and MAO-B, each with distinct substrate preferences and tissue distributions.

MAO-A preferentially metabolizes serotonin, norepinephrine, and dopamine, while MAO-B is mainly responsible for breaking down phenethylamines and benzylamines, as well as dopamine in some cases. Inhibition of these enzymes can lead to increased neurotransmitter levels in the synaptic cleft, which has implications for various psychiatric and neurological conditions, such as depression and Parkinson's disease. However, MAO inhibitors must be used with caution due to their potential to cause serious adverse effects, including hypertensive crises, when combined with certain foods or medications containing dietary amines or sympathomimetic agents.

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.

3,4-Dihydroxyphenylacetic Acid (3,4-DOPAC) is a major metabolite of dopamine, which is a neurotransmitter in the brain. Dopamine is metabolized by the enzyme monoamine oxidase to form dihydroxyphenylacetaldehyde, which is then further metabolized to 3,4-DOPAC by the enzyme aldehyde dehydrogenase.

3,4-DOPAC is found in the urine and can be used as a marker for dopamine turnover in the brain. Changes in the levels of 3,4-DOPAC have been associated with various neurological disorders such as Parkinson's disease and schizophrenia. Additionally, 3,4-DOPAC has been shown to have antioxidant properties and may play a role in protecting against oxidative stress in the brain.

Homovanillic acid (HVA) is a major metabolite of dopamine, a neurotransmitter in the human body. It is formed in the body when an enzyme called catechol-O-methyltransferase (COMT) breaks down dopamine. HVA can be measured in body fluids such as urine, cerebrospinal fluid, and plasma to assess the activity of dopamine and the integrity of the dopaminergic system. Increased levels of HVA are associated with certain neurological disorders, including Parkinson's disease, while decreased levels may indicate dopamine deficiency or other conditions affecting the nervous system.

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.

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.

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.

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.

I'm happy to help! However, it seems like there are two terms combined into one request: "Mitochondria" and "Heart." I will provide separate definitions for each.

Mitochondrion (singular) or Mitochondria (plural): These are specialized structures found in the cytoplasm of most eukaryotic cells (cells with a true nucleus), including human cells. They are often referred to as the "powerhouse" of the cell because they generate energy in the form of ATP (adenosine triphosphate) through a process called oxidative phosphorylation. Mitochondria contain their own DNA, which is distinct from the nuclear DNA, and are believed to have originated from ancient bacteria that established a symbiotic relationship with primitive eukaryotic cells.

Heart: In human anatomy, the heart is a muscular organ responsible for pumping blood throughout the body. It is located in the thoracic cavity, slightly left of the center, and is enclosed by the pericardium, a double-walled sac that provides protection and lubrication for the heart's movement. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it to the rest of the body. The heart's pumping action is regulated by electrical signals that originate in a group of specialized cardiac muscle cells called the sinoatrial node (SA node).

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.

Monoamine oxidase inhibitors (MAOIs) are a class of drugs that work by blocking the action of monoamine oxidase, an enzyme found in the brain and other organs of the body. This enzyme is responsible for breaking down certain neurotransmitters, such as serotonin, dopamine, and norepinephrine, which are chemicals that transmit signals in the brain.

By inhibiting the action of monoamine oxidase, MAOIs increase the levels of these neurotransmitters in the brain, which can help to alleviate symptoms of depression and other mood disorders. However, MAOIs also affect other chemicals in the body, including tyramine, a substance found in some foods and beverages, as well as certain medications. As a result, MAOIs can have serious side effects and interactions with other substances, making them a less commonly prescribed class of antidepressants than other types of drugs.

MAOIs are typically used as a last resort when other treatments for depression have failed, due to their potential for dangerous interactions and side effects. They require careful monitoring and dosage adjustment by a healthcare provider, and patients must follow strict dietary restrictions while taking them.

Dopamine plasma membrane transport proteins, also known as dopamine transporters (DAT), are a type of protein found in the cell membrane that play a crucial role in the regulation of dopamine neurotransmission. They are responsible for the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron, thereby terminating the signal transduction of dopamine and regulating the amount of dopamine available for further release.

Dopamine transporters belong to the family of sodium-dependent neurotransmitter transporters and are encoded by the SLC6A3 gene in humans. Abnormalities in dopamine transporter function have been implicated in several neurological and psychiatric disorders, including Parkinson's disease, attention deficit hyperactivity disorder (ADHD), and substance use disorders.

In summary, dopamine plasma membrane transport proteins are essential for the regulation of dopamine neurotransmission by mediating the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron.

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.

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.

Cyclosporine is a medication that belongs to a class of drugs called immunosuppressants. It is primarily used to prevent the rejection of transplanted organs, such as kidneys, livers, and hearts. Cyclosporine works by suppressing the activity of the immune system, which helps to reduce the risk of the body attacking the transplanted organ.

In addition to its use in organ transplantation, cyclosporine may also be used to treat certain autoimmune diseases, such as rheumatoid arthritis and psoriasis. It does this by suppressing the overactive immune response that contributes to these conditions.

Cyclosporine is available in capsule, oral solution, and injectable forms. Common side effects of the medication include kidney problems, high blood pressure, tremors, headache, and nausea. Long-term use of cyclosporine can also increase the risk of certain types of cancer and infections.

It is important to note that cyclosporine should only be used under the close supervision of a healthcare provider, as it requires regular monitoring of blood levels and kidney function.

Levodopa, also known as L-dopa, is a medication used primarily in the treatment of Parkinson's disease. It is a direct precursor to the neurotransmitter dopamine and works by being converted into dopamine in the brain, helping to restore the balance between dopamine and other neurotransmitters. This helps alleviate symptoms such as stiffness, tremors, spasms, and poor muscle control. Levodopa is often combined with carbidopa (a peripheral decarboxylase inhibitor) to prevent the conversion of levodopa to dopamine outside of the brain, reducing side effects like nausea and vomiting.

Mazindol is a prescription medication that belongs to a class of drugs known as sympathomimetic amines or anorectics. It has been used in the treatment of obesity, as it works by reducing appetite and increasing the amount of energy that the body uses. Mazindol affects certain chemicals in the brain that control appetite.

It's important to note that mazindol is not commonly used today due to its potential for abuse and serious side effects. It should only be used under the close supervision of a healthcare provider, and its use is typically reserved for individuals with severe obesity who have not responded to other treatment options.

Callithrix is a genus of New World monkeys, also known as marmosets. They are small, active primates found in the forests of South and Central America. The term "Callithrix" itself is derived from the Greek words "kallis" meaning beautiful and "thrix" meaning hair, referring to their thick, vibrantly colored fur.

Marmosets in the genus Callithrix are characterized by their slender bodies, long, bushy tails, and specialized dental structures that allow them to gouge tree bark to extract sap and exudates, which form a significant part of their diet. They also consume fruits, insects, and small vertebrates.

Some well-known species in this genus include the common marmoset (Callithrix jacchus), the white-headed marmoset (Callithrix geoffroyi), and the buffy-tufted-ear marmoset (Callithrix aurita). Marmosets are popular subjects of research due to their small size, short gestation period, and ease of breeding in captivity.

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.

Pyridinium compounds are organic salts that contain a positively charged pyridinium ion. Pyridinium is a type of cation that forms when pyridine, a basic heterocyclic organic compound, undergoes protonation. The nitrogen atom in the pyridine ring accepts a proton (H+) and becomes positively charged, forming the pyridinium ion.

Pyridinium compounds have the general structure of C5H5NH+X-, where X- is an anion or negatively charged ion. These compounds are often used in research and industry, including as catalysts, intermediates in chemical synthesis, and in pharmaceuticals. Some pyridinium compounds have been studied for their potential therapeutic uses, such as in the treatment of bacterial infections or cancer. However, it is important to note that some pyridinium compounds can also be toxic or reactive, so they must be handled with care.

Maneb is not a term that has a widely accepted medical definition. However, in the field of agriculture and toxicology, Maneb is a commonly used fungicide to control various plant diseases. It is a complex organometallic compound containing manganese.

In some contexts, Maneb may be mentioned in relation to human health because it has been found to have potential reproductive and developmental effects, as well as being potentially carcinogenic. However, it is not considered a medical term or diagnosis. If you have any concerns about exposure to Maneb or its potential health effects, it would be best to consult with a healthcare professional.

Manganese poisoning, also known as manganism, is a condition that results from excessive exposure to manganese. Manganese is an essential nutrient, but at high levels, it can become toxic to the body. The symptoms of manganese poisoning can be similar to those of Parkinson's disease and may include tremors, difficulty walking, and mood changes. In severe cases, manganese poisoning can lead to irreversible neurological damage. Exposure to manganese can occur through inhalation, ingestion, or skin contact, and is often associated with occupational exposure in industries such as welding, mining, and manufacturing of batteries and fertilizers.

I apologize for any confusion, but "Zineb" is not a medical term or concept that I am familiar with in the field of medicine. Zineb is actually a pesticide that contains the active ingredient ferbam, which is used to control fungi on crops such as grapes, apples, and potatoes. It is not a term used within the context of medical definitions or human health. I hope this clarifies any confusion. If you have any questions related to medicine or healthcare, I would be happy to try and help answer them for you.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

Manganese is not a medical condition, but it's an essential trace element that is vital for human health. Here is the medical definition of Manganese:

Manganese (Mn) is a trace mineral that is present in tiny amounts in the body. It is found mainly in bones, the liver, kidneys, and pancreas. Manganese helps the body form connective tissue, bones, blood clotting factors, and sex hormones. It also plays a role in fat and carbohydrate metabolism, calcium absorption, and blood sugar regulation. Manganese is also necessary for normal brain and nerve function.

The recommended dietary allowance (RDA) for manganese is 2.3 mg per day for adult men and 1.8 mg per day for adult women. Good food sources of manganese include nuts, seeds, legumes, whole grains, green leafy vegetables, and tea.

In some cases, exposure to high levels of manganese can cause neurological symptoms similar to Parkinson's disease, a condition known as manganism. However, this is rare and usually occurs in people who are occupationally exposed to manganese dust or fumes, such as welders.

Facilitated diffusion is a type of passive transport that involves the movement of molecules or ions across a biological membrane with the assistance of a transport protein. Unlike simple diffusion, which occurs spontaneously down a concentration gradient, facilitated diffusion allows for the movement of substances against a concentration gradient, although it does not directly consume energy.

In facilitated diffusion, the transport protein binds to the substance (also known as the solute) on one side of the membrane and then changes shape, releasing the solute on the other side. This process can increase the rate of diffusion by providing a more efficient pathway for the solute to move through the membrane.

Examples of substances that use facilitated diffusion include glucose, amino acids, and ions such as sodium and potassium. These substances are too large or too polar to pass through the hydrophobic interior of the lipid bilayer that makes up the cell membrane, so they rely on transport proteins to help them move across the membrane.

It's important to note that facilitated diffusion is a passive process and does not require energy input from the cell. However, it is a regulated process, as the number of transport proteins in the membrane can be adjusted to control the rate of solute movement.

Dyskinesias are a type of movement disorder characterized by involuntary, erratic, and often repetitive muscle movements. These movements can affect any part of the body and can include twisting, writhing, or jerking motions, as well as slow, writhing contortions. Dyskinesias can be caused by a variety of factors, including certain medications (such as those used to treat Parkinson's disease), brain injury, stroke, infection, or exposure to toxins. They can also be a side effect of some medical treatments, such as radiation therapy or chemotherapy.

Dyskinesias can have a significant impact on a person's daily life, making it difficult for them to perform routine tasks and affecting their overall quality of life. Treatment for dyskinesias depends on the underlying cause and may include medication adjustments, surgery, or physical therapy. In some cases, dyskinesias may be managed with the use of assistive devices or by modifying the person's environment to make it easier for them to move around.

Because MPTP itself is not directly harmful, toxic effects of acute MPTP poisoning can be mitigated by the administration of ... MPTP itself is not toxic, and as a lipophilic compound can cross the blood-brain barrier. Once inside the brain, MPTP is ... Erowid MPTP Vault - Contains information regarding MPTP as a neurotoxin PBS NOVA episode, "The Case of the Frozen Addict"https ... Injection of MPTP causes rapid onset of Parkinsonism, hence users of MPPP contaminated with MPTP will develop these symptoms. ...
... mptp poisoning MeSH C10.228.140.079.862.800.600 - parkinson disease, postencephalitic MeSH C10.228.140.079.882 - supranuclear ... arsenic poisoning MeSH C10.720.475.400 - lead poisoning, nervous system MeSH C10.720.475.400.350 - lead poisoning, nervous ... mptp poisoning MeSH C10.228.662.600.700.500 - parkinson disease, postencephalitic MeSH C10.228.662.700 - supranuclear palsy, ... manganese poisoning MeSH C10.720.475.600 - mercury poisoning, nervous system MeSH C10.720.475.600.150 - acrodynia MeSH C10.886. ...
... and some forms of chemical poisoning such as MPTP, can lead to substantial cell loss, producing a parkinsonian syndrome that is ... Quinones and free radicals produced by autoxidation of dopamine can poison cells, and there is evidence that this mechanism may ...
... mptp poisoning MeSH C21.613.705.600 - neuroleptic malignant syndrome MeSH C21.613.756.262 - ergotism MeSH C21.613.756.375 - ... mushroom poisoning MeSH C21.613.415.738 - salmonella food poisoning MeSH C21.613.415.846 - staphylococcal food poisoning MeSH ... lead poisoning, nervous system MeSH C21.613.589.500.400 - lead poisoning, nervous system, adult MeSH C21.613.589.500.700 - lead ... poisoning, nervous system, childhood MeSH C21.613.647.500 - mercury poisoning, nervous system MeSH C21.613.647.500.100 - ...
... arises in the body as the toxic metabolite of the closely related compound MPTP. MPTP is converted in the brain into MPP+ ... This paper followed a string of poisonings that took place in San Jose, California in 1982 in which users of an illicitly ... The oxidation of MPTP to MPP+ is a process that can be catalyzed only by MAO-B, and cells that express other forms of MAO do ... MPTP itself is not cytotoxic, however, and must be metabolized to MPP+ by MAO-B to show any signs of toxicity. ...
The term "curare" is ambiguous because it has been used to describe a number of poisons which at the time of naming were ... MPP+, the toxic metabolite of MPTP is a selective neurotoxin which interferes with oxidative phosphorylation in mitochondria by ... TTX can be fatal if consumed, and has become a common form of poisoning in many countries. Common symptoms of TTX consumption ... In the past the characterization has meant poisons used by South American tribes on arrows or darts, though it has matured to ...
In the early 1960s norbormide was developed to serve as a non-anticoagulant rat poison. During the 1970s, however, the ... Recent studies present NRB's ability to activate the mitochondrial permeability transition pore (MPTP) in isolated rat ... that such an abnormity in the mitochondrial membranes bring about issues in the cellular metabolism of the poisoned animal. The ...
Watanabe Y, Himeda T, Araki T (January 2005). "Mechanisms of MPTP toxicity and their implications for therapy of Parkinson's ... Poisoning & Drug Overdose. 6th ed. New York: McGraw-Hill; 2012. http://www.accessmedicine.com/content.aspx?aID=55982958. ... Annonaceae Carbon monoxide Carbon disulfide Cyanide Ethanol Hexane Mercury Methanol MPTP Rotenone Toluene (inhalant abuse: " ...
MPTP may be accidentally produced during the manufacture of MPPP. 1-Methyl-4-phenylpyridinium (MPP+), a metabolite of MPTP, ... More of his books deal with other aspects of clandestine chemistry, including explosives, and poisons. Fester is, however, ...
6-Hydroxydopamine MPTP Norsalsolinol Rotenone Aizawa H (2 December 2012). Metabolic Maps of Pesticides. Elsevier Science. pp. ... The patient had a history of eating fenpropathrin-poisoned fish for 6 months. The follow-up Dopaminergic degeneration study was ... "The importance of nerve terminal depolarization in pyrethroid poisoning of insects". Pesticide Biochemistry and Physiology. 20 ...
MPP+ is produced by monoamine oxidase B as a metabolite of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), and its ... "nervous tissue poisoning". Batrachotoxin Cytotoxicity Multiple chemical sensitivity Nephrotoxicity Ototoxicity Penitrem A ... The neurotoxicity of MPP+ was first investigated after MPTP was produced as a contaminant in the pethidine synthesized by a ... Jackson-Lewis, Vernice; Przedborski, Serge (Jan 2007). "Protocol for the MPTP mouse model of Parkinson's disease". Nature ...
"The protective effect of Mucuna pruriens seeds against snake venom poisoning". Journal of Ethnopharmacology. 123 (2): 356-8. ... "Mucuna pruriens Protects against MPTP Intoxicated Neuroinflammation in Parkinson's Disease through NF-κB/pAKT Signaling ...
The neurotoxin MPTP had been known earlier to cause PD-like symptoms (in humans and other primates, though not in rats) by ... Peter Fimrite (2007-10-02). "Lake poisoning seems to have worked to kill invasive pike". San Francisco Chronicle. Rytwinski T, ... Both MPTP and rotenone are lipophilic and can cross the blood-brain barrier. In 2010, a study was published detailing the ... Further studies involving MPTP have failed to show development of Lewy bodies, a key component to PD pathology. However at ...
Another common symptom of Bongkrek acid poisoning is limb soreness. In the first reported BA poisoning case in Africa, 12/17 ... known as MPTP. Bongkrek acid is permeable through this membrane and binds to the surface of ANT, inhibiting ANT's translocation ... The symptoms of Bongkrek acid poisoning are like other mitochondrial toxins. The common symptoms of Bongkrek acid poisoning are ... started to find the cause of the poisoning in the early 1930s. They successfully identified the source of poisoning, which was ...
In August 2021, MPTP Productions announced an Off-Broadway performance of the play, with Mora performing as the narrator, ... songwriter and was signed to Tricky's Massive Attack label Durban Poison/ DreamWorks S.K.G in the trip-hop group, The Autumn ...
... metabolizes into an MPTP-like compound, but is unlikely to exert neurotoxicity. Efflux by P-glycoprotein also ... an analysis of 216 poison center reports". Journal of Toxicology. Clinical Toxicology. 35 (1): 11-9. doi:10.3109/ ...
MPTP) was discovered. MPTP is able to cross the blood brain barrier and enter acidic lysosomes. MPTP is biologically activated ... and the competitive form of poisoning (which can include any of the aforementioned types). In competitive inhibition of enzyme ... Later, it was discovered that MPTP causes symptoms similar to that of Parkinson's disease. Cells in the central nervous system ... However, competitive inhibition of the MAO-B enzyme or the dopamine transporter protects against the oxidation of MPTP to MPP+ ...
One, MPPP, was found in some cases to contain an impurity called MPTP, which caused brain damage that could result in a ... Andreasen MF, Telving R, Birkler RI, Schumacher B, Johannsen M (2009). "A fatal poisoning involving Bromo-Dragonfly". Forensic ...
Poisoning is also known in animals, and some toxicity information is available for veterinary treatment. Serotonin reuptake ... January 2018). "Neuroprotective Effects of Antidepressants via Upregulation of Neurotrophic Factors in the MPTP Model of ... However, case reports of SSRI poisoning have indicated that severe toxicity can occur and deaths have been reported following ...
Because MPTP itself is not directly harmful, toxic effects of acute MPTP poisoning can be mitigated by the administration of ... MPTP itself is not toxic, and as a lipophilic compound can cross the blood-brain barrier. Once inside the brain, MPTP is ... Erowid MPTP Vault - Contains information regarding MPTP as a neurotoxin PBS NOVA episode, "The Case of the Frozen Addict"https ... Injection of MPTP causes rapid onset of Parkinsonism, hence users of MPPP contaminated with MPTP will develop these symptoms. ...
... the active metabolite of MPTP in adult rats, potentiated the toxic effects of MPTP and MPP+ on nigral neurones. Our data show ... Glutathione depletion potentiates MPTP and MPP+ toxicity in nigral dopaminergic neurones Neuroreport. 1996 Mar 22;7(4):921-3. ... MPTP Poisoning* * Mice * Mice, Inbred C57BL * Nerve Degeneration / physiology * Neurons / drug effects* ... However, the combination of BSO with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) in preweanling mice and the ...
ENVENENAMIENTO POR MPTP. MPTP POISONING. INTOXICAÇÃO POR MPTP. ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO. LEAD POISONING, ... MANGANESE POISONING. INTOXICAÇÃO POR MANGANÊS. ENVENENAMIENTO POR MERCURIO DEL SISTEMA NERVIOSO. MERCURY POISONING, NERVOUS ... LEAD POISONING, NERVOUS SYSTEM, ADULT. INTOXICAÇÃO DO SISTEMA NERVOSO POR CHUMBO EM ADULTOS. ... LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD. INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO NA INFÂNCIA. ...
ENVENENAMIENTO POR MPTP. MPTP POISONING. INTOXICAÇÃO POR MPTP. ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO. LEAD POISONING, ... MANGANESE POISONING. INTOXICAÇÃO POR MANGANÊS. ENVENENAMIENTO POR MERCURIO DEL SISTEMA NERVIOSO. MERCURY POISONING, NERVOUS ... LEAD POISONING, NERVOUS SYSTEM, ADULT. INTOXICAÇÃO DO SISTEMA NERVOSO POR CHUMBO EM ADULTOS. ... LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD. INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO NA INFÂNCIA. ...
ENVENENAMIENTO POR MPTP. MPTP POISONING. INTOXICAÇÃO POR MPTP. ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO. LEAD POISONING, ... MANGANESE POISONING. INTOXICAÇÃO POR MANGANÊS. ENVENENAMIENTO POR MERCURIO DEL SISTEMA NERVIOSO. MERCURY POISONING, NERVOUS ... LEAD POISONING, NERVOUS SYSTEM, ADULT. INTOXICAÇÃO DO SISTEMA NERVOSO POR CHUMBO EM ADULTOS. ... LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD. INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO NA INFÂNCIA. ...
MPTP POISONING ENVENENAMIENTO POR MPTP INTOXICAÇÃO POR MPTP MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE ESCLEROSIS MULTIPLE CRONICA ... MANGANESE POISONING ENVENENAMIENTO POR MANGANESO INTOXICAÇÃO POR MANGANÊS MAP KINASE KINASE KINASES QUINASAS QUINASA QUINASA ... HEAVY METAL POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR METAL PESADO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR ... LEAD POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO ...
MPTP POISONING ENVENENAMIENTO POR MPTP INTOXICAÇÃO POR MPTP MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE ESCLEROSIS MULTIPLE CRONICA ... MANGANESE POISONING ENVENENAMIENTO POR MANGANESO INTOXICAÇÃO POR MANGANÊS MAP KINASE KINASE KINASES QUINASAS QUINASA QUINASA ... HEAVY METAL POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR METAL PESADO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR ... LEAD POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO ...
INTOXICAÇÃO POR MPTP MPTP POISONING ENVENENAMIENTO POR MPTP ISQUEMIA DO CORDÃO ESPINHAL SPINAL CORD ISCHEMIA ISQUEMIA DE LA ... ARSENIC POISONING ENVENENAMIENTO POR ARSENICO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO LEAD POISONING, NERVOUS SYSTEM ... MERCURY POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR MERCURIO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR METAL ... LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO EN LA INFANCIA ...
ENVENENAMIENTO POR MPTP. MPTP POISONING. INTOXICAÇÃO POR MPTP. ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO. LEAD POISONING, ... MANGANESE POISONING. INTOXICAÇÃO POR MANGANÊS. ENVENENAMIENTO POR MERCURIO DEL SISTEMA NERVIOSO. MERCURY POISONING, NERVOUS ... LEAD POISONING, NERVOUS SYSTEM, ADULT. INTOXICAÇÃO DO SISTEMA NERVOSO POR CHUMBO EM ADULTOS. ... LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD. INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO NA INFÂNCIA. ...
MPTP POISONING ENVENENAMIENTO POR MPTP INTOXICAÇÃO POR MPTP MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE ESCLEROSIS MULTIPLE CRONICA ... MANGANESE POISONING ENVENENAMIENTO POR MANGANESO INTOXICAÇÃO POR MANGANÊS MAP KINASE KINASE KINASES QUINASAS QUINASA QUINASA ... HEAVY METAL POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR METAL PESADO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR ... LEAD POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO ...
INTOXICAÇÃO POR MPTP MPTP POISONING ENVENENAMIENTO POR MPTP ISQUEMIA DO CORDÃO ESPINHAL SPINAL CORD ISCHEMIA ISQUEMIA DE LA ... ARSENIC POISONING ENVENENAMIENTO POR ARSENICO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO LEAD POISONING, NERVOUS SYSTEM ... MERCURY POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR MERCURIO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR METAL ... LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO EN LA INFANCIA ...
MPTP POISONING ENVENENAMIENTO POR MPTP INTOXICAÇÃO POR MPTP MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE ESCLEROSIS MULTIPLE CRONICA ... MANGANESE POISONING ENVENENAMIENTO POR MANGANESO INTOXICAÇÃO POR MANGANÊS MAP KINASE KINASE KINASES QUINASAS QUINASA QUINASA ... HEAVY METAL POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR METAL PESADO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR ... LEAD POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO ...
MPTP POISONING ENVENENAMIENTO POR MPTP INTOXICAÇÃO POR MPTP MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE ESCLEROSIS MULTIPLE CRONICA ... MANGANESE POISONING ENVENENAMIENTO POR MANGANESO INTOXICAÇÃO POR MANGANÊS MAP KINASE KINASE KINASES QUINASAS QUINASA QUINASA ... HEAVY METAL POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR METAL PESADO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR ... LEAD POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO ...
INTOXICAÇÃO POR MPTP MPTP POISONING ENVENENAMIENTO POR MPTP ISQUEMIA DO CORDÃO ESPINHAL SPINAL CORD ISCHEMIA ISQUEMIA DE LA ... ARSENIC POISONING ENVENENAMIENTO POR ARSENICO INTOXICAÇÃO POR CHUMBO DO SISTEMA NERVOSO LEAD POISONING, NERVOUS SYSTEM ... MERCURY POISONING, NERVOUS SYSTEM ENVENENAMIENTO POR MERCURIO DEL SISTEMA NERVIOSO INTOXICAÇÃO DO SISTEMA NERVOSO POR METAL ... LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD ENVENENAMIENTO POR PLOMO DEL SISTEMA NERVIOSO EN LA INFANCIA ...
6: MPTP Poisoning Links A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal ... 5: Manganese Poisoning Links Manganese poisoning is associated with chronic inhalation of manganese particles by individuals ... MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ...
Animals, Deep Brain Stimulation, Female, Globus Pallidus, MPTP Poisoning, Neurons, Pedunculopontine Tegmental Nucleus ...
... carbon monoxide poisoning, or MPTP (a byproduct of heroin usage). ...
poisoning:MPTP Poisoning toxicity:MPTP Poisoning Date Established. 1990/01/01. Date of Entry. 1989/05/25. Revision Date. 2016/ ... MPTP N-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Pharm Action. Neurotoxins. Dopamine Agents. Registry Number. 9P21XSP91P. ... poisoning:MPTP Poisoning toxicity:MPTP Poisoning Allowable Qualifiers. * administration & dosage (AD) * adverse effects (AE) ...
MPTP Poisoning. *Neuroleptic Malignant Syndrome. Below are MeSH descriptors whose meaning is more specific than "Neuroleptic ...
MPTP Poisoning [C10.228.140.079.862.800.300] * Parkinson Disease, Postencephalitic [C10.228.140.079.862.800.600] ...
... mitochondrial poisons, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone, lead to degeneration of ... Clinical and experimental MPTP observations in the early 1980s fuelled the search for environmental toxins potentially ... carbon monoxide after acute poisoning, cyanide, n-hexane and other chemical toxicity may include features mimicking ... implicated in PD; paraquat, a herbicide chemically similar to MPTP, was perhaps the first of a series of such hypotheses ...
Heavy Metal Poisoning, Nervous System. *MPTP Poisoning. *Neuroleptic Malignant Syndrome. Below are MeSH descriptors whose ...
Throughout the millennia, poisons have played an important role involves the dopaminergic neurons phencyclidine mptp ... Foodborne poisoning with colchicine. Providesfort and aids (p. In general, ocular injury can guide caregivers in the synthesis ... Purine analogs and pyrimidine analogs (eg,. Routine testing for copper poisoning; it also became mainstays of treatment. ... 20 centuries after socrates was executed by poison control centers regarding deet exposures involve minor or no symptoms, and ...
ATPase by cardiac glycosides has been shown to potentiate toxic effects of excitatory amino acids and mitochondrial poisons in ... MPTP) in vivo. Mice were injected with digoxin (1 mg/kg) or vehicle followed by MPTP (20 mg/kg) or saline 1 h later. After 1 or ... MPTP) in vivo. Mice were injected with digoxin (1 mg/kg) or vehicle followed by MPTP (20 mg/kg) or saline 1 h later. After 1 or ... MPTP) in vivo. Mice were injected with digoxin (1 mg/kg) or vehicle followed by MPTP (20 mg/kg) or saline 1 h later. After 1 or ...
Several toxins like illegal drugs contaminated with a chemical called MPTP may cause severe Parkinson-like symptoms. It was ... severe carbon monoxide (CO) poisoning. They also include the insecticides permethrin and beta-hexachlorocyclohexane (beta-HCH ... found that once MPTP crossed into the brain it started killing brain cells. ...
"Mechanisms of MPTP toxicity and their implications for therapy of Parkinsons disease" (PDF). Medical Science Monitor. 11 (1 ... Poisoning & Drug Overdose. 6th ed. New York: McGraw-Hill; 2012. http://www.accessmedicine.com/content.aspx?aID=55982958. ...
... and some forms of chemical poisoning such as MPTP, can lead to substantial cell loss, producing a parkinsonian syndrome that is ... Quinones and free radicals produced by autoxidation of dopamine can poison cells, and there is evidence that this mechanism may ...
MPTP, a drug that sometimes contaminates heroin, can suddenly cause a severe and irreversible form of Parkinsons. This drug ... carbon monoxide or manganese poisoning.. The researchers also noted that many changes occur in the brains of people with ...
MPTP Neurotoxicity Syndrome MPTP Neurotoxicity Syndromes MPTP Poisoning MPTP-Induced Degeneration of the Striatum MPTP-Induced ... MPTP Induced Degeneration of the Striatum MPTP Induced Experimental Parkinsonism MPTP Induced Parkinsonism ...
  • A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. (neurotalk.org)
  • Inhibition of Na + /K + ATPase by cardiac glycosides has been shown to potentiate toxic effects of excitatory amino acids and mitochondrial poisons in neurons in vitro. (elsevierpure.com)
  • carbon monoxide or manganese poisoning. (annvio.com)
  • The FDA currently only recognizes the use of Methylene Blue for treatment of: methemoglobinemia, cyanide poisoning, septic shock, urinary tract infection (prevention,) and carbon monoxide poisoning. (thearcanum.io)
  • however, most of the recent studies indicate that MPTP can result in Parkinsonism-like syndromes in mice (especially chronic syndromes). (wikipedia.org)
  • However, the combination of BSO with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) in preweanling mice and the combination of nigral injections of BSO with intrastriatal injections of MPP+ (1-methyl-4-phenylpyridinium), the active metabolite of MPTP in adult rats, potentiated the toxic effects of MPTP and MPP+ on nigral neurones. (nih.gov)
  • The purpose of the current study was to evaluate the effects of an MPTP-induced dopaminergic lesion in mice on social odor recognition (SOR) memory. (unboundmedicine.com)
  • Mice were acutely treated with MPTP and evaluated for memory impairments in the SOR assay and characterized using biochemical and immunohistochemical methods approximately 2 weeks later. (unboundmedicine.com)
  • MPTP treatment of C57BL/6N mice produced a profound decrease in dopamine levels, dopamine transporter binding and tyrosine hydroxylase immunoreactivity in the striatum. (unboundmedicine.com)
  • Mice were injected with digoxin (1 mg/kg) or vehicle followed by MPTP (20 mg/kg) or saline 1 h later. (elsevierpure.com)
  • MPTP caused a significant 35-45% reduction in striatal dopamine levels compared to those in control mice. (elsevierpure.com)
  • found that when this variant form of ATP5G1 was introduced into the cells of mice, their mitochondria was better at coping with stress conditions, such as low oxygen, low temperature and poisoning. (elifesciences.org)
  • Manganese poisoning is associated with chronic inhalation of manganese particles by individuals who work with manganese ore. (neurotalk.org)
  • The neurotoxicity of MPTP was hinted at in 1976 after Barry Kidston, a 23-year-old chemistry graduate student in Maryland, US, synthesized MPPP with MPTP as a major impurity and self-injected the result. (wikipedia.org)
  • This result was unexpected and suggests that cardiac glycosides may protect against MPTP neurotoxicity. (elsevierpure.com)
  • The present study tested the hypothesis that the systemic administration of the cardiac glycoside, digoxin, potentiates effects of the dopamine neurotoxin 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) in vivo. (elsevierpure.com)
  • However, pretreatment with digoxin completely prevented the MPTP-induced dopamine depletion. (elsevierpure.com)
  • Inhibiting c-JNKs or their upstream signals may reduce dopamine- mediated neuronal death induced at near MPTP, suggesting a possible medicinal appli- cation for c-JNK inhibitors in PD (Depression et al. (ozdifferent.sk)
  • MAOIs prevent the metabolism of MPTP to MPP+ by inhibiting the action of MAO-B, minimizing toxicity, and preventing neural death. (wikipedia.org)
  • MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (neurotalk.org)
  • In 1983, four people in Santa Clara County, California, US, were diagnosed with Parkinsonism after having used MPPP contaminated with MPTP, and as many as 120 were reported to have been diagnosed with Parkinson's symptoms. (wikipedia.org)
  • 1984) found that injections of MPTP in squirrel monkeys resulted in Parkinsonism, symptoms of which were subsequently reduced by levodopa, the drug-of-choice in the treatment of Parkinson's disease along with carbidopa and entacapone. (wikipedia.org)
  • MPTP, a drug that sometimes contaminates heroin, can suddenly cause a severe and irreversible form of Parkinson's. (annvio.com)
  • Animal Aid has uncovered two shocking charity-funded experiments that involved monkeys being brain-damaged through the use of a toxic chemical called MPTP, overdosed with a Parkinson's disease (PD) drug to induce debilitating side effects, and given the street drug ecstasy, or a derivative. (victimsofcharity.org)
  • Exposure to the toxic chemical 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has also been found to contribute to development of Parkinson's disease, a disorder that affects one's movement. (neurology-clinics.com)
  • It was contaminated with MPTP, and within three days he began exhibiting symptoms of Parkinson's disease. (umaryland.edu)
  • MPTP itself is not toxic, and as a lipophilic compound can cross the blood-brain barrier. (wikipedia.org)
  • Once inside the brain, MPTP is metabolized into the toxic cation 1-methyl-4-phenylpyridinium (MPP+) by the enzyme monoamine oxidase B (MAO-B) of glial cells, specifically astrocytes. (wikipedia.org)
  • Because MPTP itself is not directly harmful, toxic effects of acute MPTP poisoning can be mitigated by the administration of monoamine oxidase inhibitors (MAOIs) such as selegiline. (wikipedia.org)
  • Paraquat is dangerous because it's a restricted-use pesticide that's highly toxic for humans, which is why it comes with the Danger/Poison signal. (schmidtandclark.com)
  • Injection of MPTP causes rapid onset of Parkinsonism, hence users of MPPP contaminated with MPTP will develop these symptoms. (wikipedia.org)
  • MPTP causes Parkinsonism in primates, including humans. (wikipedia.org)
  • Here we demonstrate that SOR memory is sensitive to MPTP treatment and that it correlates with multiple measures of nigrostriatal integrity. (unboundmedicine.com)
  • The Home Office has confirmed that experiments in which monkeys are brain-damaged with MPTP fall into the highest category of severity. (victimsofcharity.org)
  • It has previously stated that brain-damaging monkeys with MPTP has 'devastating welfare costs' for the animals involved and serious questions arise as to whether the re-use of primates in such harmful experiments would be permitted in the UK, or in the other EU countries governed by the same European directive. (victimsofcharity.org)
  • Monkeys do not get PD, and the symptoms induced in them by brain-poisoning fail to replicate key features of the disease. (victimsofcharity.org)
  • Brain-poisoned monkeys gradually recover, whereas PD is a degenerative disease. (victimsofcharity.org)
  • Dr Marius Maxwell, an Oxford, Cambridge and Harvard-trained neurosurgeon, has strongly criticised, on scientific grounds, the use of brain-poisoned monkeys as a 'model' for PD research. (victimsofcharity.org)
  • The physicians first concern is only a temporizing measure until the 20th century, 20 centuries after socrates was executed by poison control centers regarding deet exposures involve minor or no symptoms, and ability to bear children. (oaksofwellington.com)
  • Several toxins like illegal drugs contaminated with a chemical called MPTP may cause severe Parkinson-like symptoms. (news-medical.net)
  • In the case of chronic alcohol abuse or lead poisoning, these symptoms (particularly cognition problems) may worsen, in which case medical attention is necessary. (neurology-clinics.com)
  • The height OSMI-1 cell line of Missouri levels throughout plant food answer triggered significant poisoning as well as plants created the symptoms. (micrornalibrary.com)
  • It is through a counterintuitive mechanism that the excess calcium in the cytosol causes the calcium WITHIN the Mitochondria to build up, opening a pore (called mPTP) in its outer membrane, allowing for the Apoptotic signaling to commence. (substack.com)
  • Rats are almost immune to the adverse effects of MPTP. (wikipedia.org)
  • Changes in the dopaminergic system parallel those observed in SOR with MPTP treatment impairing recognition memory in the absence of a deficit in odor discrimination during learning. (unboundmedicine.com)
  • However, OP poisoning cases before treatment showed significant DNA harm, and they didn't aberration display any chromosomal. (healthyconnectionsinc.com)
  • The National Institute of Mental Health found traces of MPTP and other pethidine analogs in his lab. (wikipedia.org)
  • It was found that once MPTP crossed into the brain it started killing brain cells. (news-medical.net)
  • Another study found that paraquat has a chemical structure very similar to MPTP. (schmidtandclark.com)
  • The Parkinson-inducing effects of MPTP were first discovered following accidental injection as a result of contaminated MPPP. (wikipedia.org)
  • While MPTP itself has no psychoactive effects, the compound may be accidentally produced during the manufacture of MPPP, a synthetic opioid drug with effects similar to those of morphine and pethidine (meperidine). (wikipedia.org)
  • The combination of proteomics (high-density liquid chromatography [LC] coupled to MS) with microarray analysis of the pooled left and right striata from mice previously exposed to MPTP compared with METH exposure, culminated in a large descriptive data set on proteomic changes induced by these mitochondrial poisons. (medscape.com)
  • The actual fact that poisons impacting mitochondrial function result in impairment of proteasome degradation isn't astonishing also, considering that the proteasome degradation routine is normally ATP-dependent. (innovation-ecosystems-agora.com)
  • Studies of pet types of PD induced with these poisons claim that mitochondrial dysfunction and oxidative tension are essential pathogenic systems [1]. (abt-888.net)
  • Because MPTP itself is not directly harmful, toxic effects of acute MPTP poisoning can be mitigated by the administration of monoamine oxidase inhibitors (MAOIs) such as selegiline. (wikipedia.org)
  • For example using the raising usage of methyltin as stabilizers in PVC creation in developing countries such as for example in China multiple acute poisoning incidents at work have already been reported lately (Tang 2010). (mdm2-inhibitors.com)
  • Structural similarity between MPTP and the herbicide paraquat 5 has led to speculation of a possible association between exposure to pesticides and PD. (bmj.com)
  • [ 113 ] Since this result could not be replicated in METH-treated animals, it was suggested that MPTP generates a potentially higher degree of oxidative damage and cell death than that of METH. (medscape.com)
  • Single low doses of MPTP decrease tyrosine hydroxylase expression in the absence of overt neuron loss. (omeka.net)
  • The particular developed in-situ twistable homostructure products permit thorough investigation with the pose angle results within a unit, hence might largely progress your research involving twistronics.Cholera toxic (CT) and Escherichia coli heat-labile enterotoxin (LT) are usually structurally comparable AB5-type necessary protein poisons. (sirtuinsignaling.com)