The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.
An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
Ergostane derivatives of 28 carbons with oxygens at C1, C22, and C26 positions and the side chain cyclized. They are found in WITHANIA plant genus and have cytotoxic and other effects.
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.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A rare form of DEMENTIA that is sometimes familial. Clinical features include APHASIA; APRAXIA; CONFUSION; ANOMIA; memory loss; and personality deterioration. This pattern is consistent with the pathologic findings of circumscribed atrophy of the poles of the FRONTAL LOBE and TEMPORAL LOBE. Neuronal loss is maximal in the HIPPOCAMPUS, entorhinal cortex, and AMYGDALA. Some ballooned cortical neurons contain argentophylic (Pick) bodies. (From Brain Pathol 1998 Apr;8(2):339-54; Adams et al., Principles of Neurology, 6th ed, pp1057-9)
A calcium-binding protein that is 92 AA long, contains 2 EF-hand domains, and is concentrated mainly in GLIAL CELLS. Elevation of S100B levels in brain tissue correlates with a role in neurological disorders.
Retinal diseases refer to a diverse group of vision-threatening disorders that affect the retina's structure and function, including age-related macular degeneration, diabetic retinopathy, retinal detachment, retinitis pigmentosa, and macular edema, among others.
The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.
Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.
The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.
Devices for examining the interior of the eye, permitting the clear visualization of the structures of the eye at any depth. (UMDNS, 1999)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
A metabolite in the principal biochemical pathway of lysine. It antagonizes neuroexcitatory activity modulated by the glutamate receptor, N-METHYL-D-ASPARTATE; (NMDA).
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.
(2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.
Neurologic disorders caused by exposure to toxic substances through ingestion, injection, cutaneous application, or other method. This includes conditions caused by biologic, chemical, and pharmaceutical agents.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
Penetrating wounds caused by a pointed object.
Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.
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.

Increased neurodegeneration during ageing in mice lacking high-affinity nicotine receptors. (1/642)

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

Oligodendroglial vacuolar degeneration in the bilateral motor cortices and astrocytosis in epileptic beagle dogs. (2/642)

We performed a pathologic examination of the brains of three dogs in an epileptic beagle colony. Histologically, all the cases had diffuse astrocytosis in the cerebral cortex and basal ganglia as well as the hippocampus, whereas they showed acute nerve cell change in the hippocampus and some other areas of the cerebrum. One of these animals showed laminar myelin pallor associated with the presence of many vacuoles in the IV to VI layers of the bilateral motor cortices. Most of the vacuoles contained fine granules stained with luxol-fast-blue stain. Ultrastructural examination revealed that some oligodendrocytes and perineuronal satellite oligodendrocytes in the bilateral cerebral motor cortices of the two affected dogs had many vacuoles surrounded by myelin-like lamellar structures. These findings suggest a possibility that astrocytosis in the cerebrum and vacuolar degeneration of oligodendrocytes in the cerebral motor cortex may be, at least in part, related to the occurrence or development of seizures.  (+info)

Cyclo-oxygenase-2 mediates P2Y receptor-induced reactive astrogliosis. (3/642)

Excessive cyclo-oxygenase-2 (COX-2) induction may play a role in chronic neurological diseases characterized by inflammation and astrogliosis. We have previously identified an astroglial receptor for extracellular nucleotides, a P2Y receptor, whose stimulation leads to arachidonic acid (AA) release, followed, 3 days later, by morphological changes resembling reactive astrogliosis. Since COX-2 may be upregulated by AA metabolites, we assessed a possible role for COX-2 in P2Y receptor-mediated astrogliosis. A brief challenge of rat astrocytes with the ATP analogue alpha,beta-methylene ATP (alpha,beta(me)ATP) resulted, 24 h later, in significantly increased COX-2 expression. The selective COX-2 inhibitor NS-398 completely abolished alpha,beta(me)ATP-induced astrocytic activation. Constitutive astroglial COX-1 or COX-2 did not play any role in purine-induced reactive astrogliosis. PGE2, a main metabolite of COX-2, also induced astrocytic activation. These data suggest that a P2Y receptor mediates reactive astrogliosis via induction of COX-2. Antagonists selective for this receptor may counteract excessive COX-2 activation in both acute and chronic neurological diseases.  (+info)

Platelet activating factor receptor expression is associated with neuronal apoptosis in an in vivo model of excitotoxicity. (4/642)

Platelet activating factor (PAF), an endogenous proinflammatory agent, mediates neuronal survival, glutamate release, and transcriptional activation following excitotoxin challenge. To determine whether PAF receptor (PAFR) expression is altered during excitotoxicity, changes in PAFR mRNA localization were compared with markers of neuronal apoptosis and reactive gliosis following systemic injection of kainic acid. Data from semi-quantitative RT-PCR, in situ hybridization, DNA fragmentation, cellular morphology analysis, and immunohistochemistry demonstrate that the localization of PAFR mRNA is altered during kainic acid-induced neurodegeneration. While PAFR mRNA is normally exhibited by neurons and microglia in rat hippocampus, expression becomes restricted to apoptotic neurons and to glia involved in phagocytosing apoptotic debris following treatment with excitotoxin. PAFR mRNA is rarely detected in surviving neurons. These data provide the first indication that PAFR-expressing neurons may be preferentially susceptible to excitotoxic challenge.  (+info)

Multifocal meningioangiomatosis: a report of two cases. (5/642)

We report the CT and MR findings in two patients with multifocal meningioangiomatosis, neither of whom had a family history or stigmata of neurofibromatosis. All lesions were located in the cortical and subcortical areas and had round dense calcifications with eccentric cysts. The masses were associated with surrounding edema and gliosis.  (+info)

Transgenic mice expressing mutated full-length HD cDNA: a paradigm for locomotor changes and selective neuronal loss in Huntington's disease. (6/642)

Huntington's disease (HD) is a progressive neurodegenerative disorder characterized clinically by motor and psychiatric disturbances and pathologically by neuronal loss and gliosis (reactive astrocytosis) particularly in the striatum and cerebral cortex. We have recently created HD full-length cDNA transgenic mouse models that may serve as a paradigm for HD. A more detailed characterization of these models is presented here. The transgene encoding normal huntingtin consists of 9417 bp of the huntingtin coding sequences including 16 tandem CAGs coding for polyglutamines as part of exon 1. The transgene is driven by a heterologous cytomegalovirus promoter. Five independent transgenic mouse lines were obtained using this construct. An additional six transgenic lines were obtained using full-length HD constructs that have been modified to include either 48 or 89 CAG repeat expansions. Southern blot and densitometric analyses indicated unique integration sites for the transgene in each of the lines with a copy number ranging from two to 22 copies. Widespread expression of the transgene in brain, heart, spleen, kidney, lung, liver and gonads from each line was determined by Western blot analyses. In the brain, transgene expression was found in cerebral cortex, striatum, hippocampus and cerebellum. Expression of the transgene was as much as five times the endogenous mouse huntingtin level. Phenotypically, only mice expressing 48 or 89 CAG repeats manifested progressive behavioural and motor dysfunction. Early behavioural abnormalities were characterized by trunk curling and clasping of both fore- and hindlimbs when the animals were suspended by their tails. Subsequently, these mice exhibited hyperkinetic movements, including heightened exploratory activities, unidirectional rotational behaviour, backflipping and excessive grooming that lasted for several weeks. Eventually, the animals progressed to a hypokinetic phase consisting of slowed movements and lack of response to sensory stimuli. Urine retention or incontinence was also a prominent feature of the hypokinetic phase. At the end stage of the disease process, HD48(B,D) and HD89(A-C) mice became akinetic just prior to death. Neuropathological examination of mice at various stages indicated that it was only during the hypokinetic phase and thereafter when selective neuronal loss was most apparent. Regions of neurodegeneration and loss included the striatum, cerebral cortex, thalamus and hippocampus. TUNEL staining indicated an apoptotic mode of cell death in these brain regions. Comparative neuronal counts after Nissl staining showed as much as 20% loss of small and medium neurons in the striatum in mice at the hypokinetic and akinetic stages. Reactive astrocytosis accompanied the areas of neurodegeneration and loss. Polyglutamine aggregates in the form of neuronal intranuclear inclusions and diffuse nuclear and perinuclear aggregations were found in a small percentage of neurons, including those in brain regions that are typically spared in HD. This observation suggests that polyglutamine aggregates may not be sufficient to cause neuronal loss in HD. In both behavioural and neuropathological analyses, wild-type and transgenic animals with 16 CAG repeats were indistinguishable from each other and do not exhibit the changes observed for mice carrying the 48 and 89 CAG repeat mutations. Thus, animals expressing the CAG repeat expansions appear to represent clinically analogous models for HD pathogenesis, and may also provide insights into the underlying pathophysiological mechanisms of other triplet repeat disorders.  (+info)

Inflammatory CNS demyelination: histopathologic correlation with in vivo quantitative proton MR spectroscopy. (7/642)

BACKGROUND AND PURPOSE: The mechanisms behind the demyelination that is characteristic of multiple sclerosis (MS) are still poorly understood. The purpose of this study was to compare immunopathologic findings in demyelinating lesions of three patients with in vivo assessments obtained by quantitative proton MR spectroscopy (MRS). METHODS: Between four and seven stereotactic needle brain biopsies were performed in three young adults with diagnostically equivocal findings for MS. Axonal density, gliosis, blood brain-barrier breakdown, and demyelinating activity of lesions were determined. Combined MR/MRS studies were performed (T1-weighted fast low-angle shot and single-voxel stimulated-echo acquisition mode), and absolute metabolite levels were obtained with a user-independent fitting routine. Metabolite control values were obtained from a group of age-matched healthy volunteers (n = 40, age range, 20-25 years old). Alterations of metabolite levels of control subjects were considered significant when exceeding two standard deviations. RESULTS: There were parallel decreases of N-acetylaspartate (21%-82%) and reductions of axonal density (44%-74%) in demyelinating plaques. Concomitant increases of choline (75%-152%) and myo-inositol (84%-160%) corresponded to glial proliferation. Elevated lactate was associated with inflammation. CONCLUSION: The present data suggest that in vivo MRS indicates key pathologic features of demyelinating lesions.  (+info)

Differential diagnosis between organic and inorganic mercury poisoning in human cases--the pathologic point of view. (8/642)

Differences in pathology were found between acute and chronic exposure to methylmercury, mercury vapor, and inorganic mercury. Characteristic pathologic changes produced by organic mercury in the brain have previously been described in patients with Minamata disease. The brains of patients who presented with acute onset of symptoms and died within 2-mo showed loss of neurons with reactive proliferation of glial cells, microcavitation, vascular congestion, petechial hemorrhage, and edema in the cerebral cortices, predominantly in the calcarine, pre- and postcentral, and transverse temporal cortices and in the cerebellar cortex. The neuropathologic changes in the patients with acute onset of symptoms who survived for a long period (>10 yr) were also included neuronal loss with reactive proliferation of glial cells in similar anatomic locations. The neuropathologic changes in patients with inorganic mercury poisoning are quite different. Autopsies performed on 3 individuals with fatal cases of acute inorganic mercury poisoning who were exposed to mercury vapor for about 2 wk revealed diffuse organized pneumonia, renal cortical necrosis, disseminated intravascular coagulopathy, and infarctions in the brain and kidneys. In 2 other patients who worked in mercury mines for about 10 yr and who suffered from chronic inorganic poisoning, no specific lesions were demonstrated in the brain. However, the assay and the histochemistry of mercury revealed that inorganic mercury was present in the brain in all 3 groups irrespective of the brain lesions and the duration of clinical signs.  (+info)

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

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

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

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

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

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

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

Some of the essential functions of astrocytes include:

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

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

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

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

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

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

Withanolides are a class of steroidal lactones found primarily in the nightshade family of plants, including Ashwagandha (Withania somnifera), a traditional Ayurvedic medicinal plant. These compounds have been reported to possess various pharmacological activities such as anti-inflammatory, antitumor, and immunomodulatory effects. They are currently being researched for their potential uses in various medical applications.

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.

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.

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

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

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

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

The S100 calcium binding protein beta subunit, also known as S100B, is a member of the S100 family of proteins. These proteins are characterized by their ability to bind calcium ions and play a role in intracellular signaling pathways. The S100B protein is made up of two subunits, alpha and beta, which form a homodimer. It is primarily expressed in astrocytes, a type of glial cell found in the central nervous system.

S100B has been shown to have both intracellular and extracellular functions. Inside cells, it regulates various processes such as the dynamics of cytoskeleton, calcium homeostasis and cell proliferation. Extracellularly, S100B acts as a damage-associated molecular pattern (DAMP) molecule, released from damaged or stressed cells, where it can interact with receptors on other cells to induce inflammatory responses, neuronal death and contribute to the pathogenesis of several neurological disorders.

Elevated levels of S100B in cerebrospinal fluid (CSF) or blood are associated with various central nervous system injuries such as traumatic brain injury, spinal cord injury, stroke, neurodegenerative diseases and some types of cancer. Therefore, it is considered a biomarker for these conditions.

Retinal diseases refer to a group of conditions that affect the retina, which is the light-sensitive tissue located at the back of the eye. The retina is responsible for converting light into electrical signals that are sent to the brain and interpreted as visual images. Retinal diseases can cause vision loss or even blindness, depending on their severity and location in the retina.

Some common retinal diseases include:

1. Age-related macular degeneration (AMD): A progressive disease that affects the central part of the retina called the macula, causing blurred or distorted vision.
2. Diabetic retinopathy: A complication of diabetes that can damage the blood vessels in the retina, leading to vision loss.
3. Retinal detachment: A serious condition where the retina becomes separated from its underlying tissue, requiring immediate medical attention.
4. Macular edema: Swelling or thickening of the macula due to fluid accumulation, which can cause blurred vision.
5. Retinitis pigmentosa: A group of inherited eye disorders that affect the retina's ability to respond to light, causing progressive vision loss.
6. Macular hole: A small break in the macula that can cause distorted or blurry vision.
7. Retinal vein occlusion: Blockage of the retinal veins that can lead to bleeding, swelling, and potential vision loss.

Treatment for retinal diseases varies depending on the specific condition and its severity. Some treatments include medication, laser therapy, surgery, or a combination of these options. Regular eye exams are essential for early detection and treatment of retinal diseases.

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

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

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

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

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

Some examples of brain diseases include:

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

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

The retina is the innermost, light-sensitive layer of tissue in the eye of many vertebrates and some cephalopods. It receives light that has been focused by the cornea and lens, converts it into neural signals, and sends these to the brain via the optic nerve. The retina contains several types of photoreceptor cells including rods (which handle vision in low light) and cones (which are active in bright light and are capable of color vision).

In medical terms, any pathological changes or diseases affecting the retinal structure and function can lead to visual impairment or blindness. Examples include age-related macular degeneration, diabetic retinopathy, retinal detachment, and retinitis pigmentosa among others.

An ophthalmoscope is a medical device used by healthcare professionals to examine the interior structures of the eye, including the retina, optic disc, and vitreous humor. It consists of a handle with a battery-powered light source and a head that contains lenses for focusing. When placed in contact with the patient's dilated pupil, the ophthalmoscope allows the examiner to visualize the internal structures of the eye and assess their health. Ophthalmoscopes are commonly used in routine eye examinations, as well as in the diagnosis and management of various eye conditions and diseases.

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

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.

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

2-Aminoadipic acid (2-AAA) is a type of amino acid that is formed as a byproduct of the metabolism of lysine, which is an essential amino acid. It is not commonly considered a building block of proteins, but it does play a role in various biochemical pathways in the body.

Abnormally high levels of 2-AAA have been found in certain medical conditions, such as genetic disorders of lysine metabolism and in some neurodegenerative diseases like multiple sclerosis and Alzheimer's disease. However, it is not currently clear whether elevated levels of 2-AAA are a cause or a consequence of these conditions.

Research is ongoing to better understand the role of 2-AAA in human health and disease.

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

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

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

A brain injury is defined as damage to the brain that occurs following an external force or trauma, such as a blow to the head, a fall, or a motor vehicle accident. Brain injuries can also result from internal conditions, such as lack of oxygen or a stroke. There are two main types of brain injuries: traumatic and acquired.

Traumatic brain injury (TBI) is caused by an external force that results in the brain moving within the skull or the skull being fractured. Mild TBIs may result in temporary symptoms such as headaches, confusion, and memory loss, while severe TBIs can cause long-term complications, including physical, cognitive, and emotional impairments.

Acquired brain injury (ABI) is any injury to the brain that occurs after birth and is not hereditary, congenital, or degenerative. ABIs are often caused by medical conditions such as strokes, tumors, anoxia (lack of oxygen), or infections.

Both TBIs and ABIs can range from mild to severe and may result in a variety of physical, cognitive, and emotional symptoms that can impact a person's ability to perform daily activities and function independently. Treatment for brain injuries typically involves a multidisciplinary approach, including medical management, rehabilitation, and supportive care.

Kainic acid is not a medical term per se, but it is a compound that has been widely used in scientific research, particularly in neuroscience. It is a type of excitatory amino acid that acts as an agonist at certain types of receptors in the brain, specifically the AMPA and kainate receptors.

Kainic acid is often used in research to study the effects of excitotoxicity, which is a process that occurs when nerve cells are exposed to excessive amounts of glutamate or other excitatory neurotransmitters, leading to cell damage or death. Kainic acid can induce seizures and other neurological symptoms in animals, making it a valuable tool for studying epilepsy and related disorders.

While kainic acid itself is not a medical treatment or diagnosis, understanding its effects on the brain has contributed to our knowledge of neurological diseases and potential targets for therapy.

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

Symptoms of neurotoxicity syndromes may include:

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

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

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

Medical Definition:

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

A stab wound is a type of penetrating trauma to the body caused by a sharp object such as a knife or screwdriver. The injury may be classified as either a stabbing or a puncture wound, depending on the nature of the object and the manner in which it was inflicted. Stab wounds typically involve a forceful thrusting motion, which can result in damage to internal organs, blood vessels, and other structures.

The depth and severity of a stab wound depend on several factors, including the type and length of the weapon used, the angle and force of the strike, and the location of the wound on the body. Stab wounds to vital areas such as the chest or abdomen can be particularly dangerous due to the risk of internal bleeding and infection.

Immediate medical attention is required for stab wounds, even if they appear minor at first glance. Treatment may involve wound cleaning, suturing, antibiotics, and in some cases, surgery to repair damaged tissues or organs. In severe cases, stab wounds can lead to shock, organ failure, and even death if left untreated.

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

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.

In such cases, gliosis may also be reversible. In all instances of gliosis resulting from CNS trauma, the long-term clinical ... but the extent and nature of the gliosis response vary widely based on the triggering insult. Gliosis in any form entails an ... Gliosis is the universal response of the CNS to tissue injury and occurs as a result of many acute conditions such as trauma, ... In this light, gliosis may be seen not only as a characteristic of many neuropathologies but as a potential contributor to, or ...
Gliosis occurs when the body creates more, or larger, glial cells that cause scars in the brain that impact body functions. The ... Astrocytes participating in gliosis are referred to as reactive astrocytes. Gemistocytic astrocytes are assumed to be intensely ... The human brain contains many cells that can impact gliosis, including endothelial progenitors, fibroblast lineage cells, ... Dabbs, David J (2019). "Gliosis - an overview , ScienceDirect Topics". www.sciencedirect.com. Retrieved 2022-04-04. Brat, ...
Current studies are researching the possible benefits of inhibiting the inflammation caused by reactive gliosis in order to ... Pekny, Milos; Nilsson, Michael (2005). "Astrocyte activation and reactive gliosis". Glia. 50 (4): 427-34. doi:10.1002/glia. ... is a classic marker for reactive gliosis. Axon regeneration does not occur in areas with an increase in GFAP and vimentin. ... and small neurotrophin that targets reactive gliosis to alleviate some neurodegenerative diseases. TGFB is a regulatory ...
Neuronal loss and gliosis are also seen. Plaques of amyloid-like material can be seen in the neocortex in some cases of CJD. ...
Xu, H.; Zhang, S. L.; Tan, G. W.; Zhu, H. W.; Huang, C. Q.; Zhang, Z. Z.; Wang, Z. X. (30 August 2012). "Reactive gliosis and ... Reactive gliosis has often referred to as the basis for neuroinflammation, which has implicated them in Alzheimer's disease and ... Członkowska, Anna; Kurkowska-Jastrzębska, Iwona (February 2011). "Inflammation and gliosis in neurological diseases - clinical ...
Huntington's disease is characterized by neuronal loss and gliosis. Symptoms of the disease include: movement disorder, ...
Damage to retinal cells induces Müller cells to produce gliosis. The result of the response varies depending on the damage and ... "Cellular signaling and factors involved in Müller cell gliosis: Neuroprotective and detrimental effects". Progress in Retinal ...
"Selective induction of astrocytic gliosis generates deficits in neuronal inhibition". Nature Neuroscience. 13 (5): 584-91. doi: ...
One of these proteins, glial fibrillary acidic protein (GFAP) can be used as a marker for reactive gliosis in damaged tissue. ... Astrocytes can also respond to CNS injury by undergoing reactive gliosis. This acts as a neuroprotective event by upregulating ...
Portions of the retina may develop gliosis as a response to injury. In the early stages, there are a few treatment options. ...
1994). "Regional differences in reactive gliosis induced by substrate-bound β-amyloid". Exp. Neurol. 130 (1): 56-66. doi: ...
Necropsy shows loss of neurons and gliosis in the caudate and globus pallidus. Similar changes may also be seen in the thalamus ...
"Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush". Investigative Ophthalmology ...
The reduced volume arises from neuronal cell loss, and increased signal arises from gliosis. The 18F-fluorodeoxyglucose PET ( ... The hippocampal neuronal cell loss and gliosis are disproportionate to the Alzheimer's disease "neuropathological change in the ... is a neuropathological condition with severe neuronal cell loss and gliosis in the hippocampus. Neuroimaging tests such as ... 8-9 Pyramidal cell loss and gliosis occurs in the CA1 sector, subiculum, entorhinal cortex, and the amygdala. ...
Formation of a septum implies that through gliosis, a membrane of glial cells has developed across the aqueduct. This abnormal ... This increased pressure amplifies the effects of gliosis, as described in the next section. With this condition, the aqueduct ... and resulting in gliosis and a proliferation of glial cells. This increased number of cells thus causes the blockage to worsen ... necessitating more pressure and velocity, and continuing the cycle of gliosis. A genetic disorder called "Brickers-Adams- ...
Diffuse gliosis may surround the large deposits but significant loss of nerve cells is rare. On electron microscopy the mineral ...
These changes are associated with diffuse gliosis, moderate loss of axons and many axonal spheroids. Activated or ameboid ...
Buffo A, Rite I, Tripathi P, Lepier A, Colak D, Horn AP, Mori T, Götz M (Mar 2008). "Origin and progeny of reactive gliosis: A ... supporting the role for OLIG2 in reactive gliosis. OLIG2 was also implicated in generating reactive astrocytes possibly in a ...
Histological examinations showed neuronal necrosis and gliosis of the cerebral cortex, cerebellum, spinal cord and brainstem. ...
These cells extend processes, and form a delicate rim of gliosis around the margin of damage. The empty space left by brain ... The brain tissue will undergo liquefactive necrosis, and a rim of gliosis will form around the damaged area. Apart from a small ...
In neonates, hypoxic injury to the cerebellum is fairly common, resulting in neuronal loss and gliosis. Symptoms of these ...
The lesions take on different forms, including areas of demyelination, spongiosis, gliosis, necrosis, and capillary ...
1995). "A role for ciliary neurotrophic factor as an inducer of reactive gliosis, the glial response to central nervous system ... A glial scar formation (gliosis) is a reactive cellular process involving astrogliosis that occurs after injury to the central ... 1991). "γ-Interferon promotes proliferation of adult human astrocytes in vitro and reactive gliosis in the adult mouse brain in ... Several main classes of molecular mediators of gliosis have been identified and are briefly discussed below. Two neuronally- ...
Histological examinations showed neuronal necrosis and gliosis of the cerebral cortex, cerebellum, spinal cord and brainstem. ...
"Neuronal preservation and reactive gliosis attenuation following neonatal sciatic nerve axotomy by a fluorinated cannabidiol ...
The mechanisms include inhibiting apoptosis of healthy cells and preventing gliosis, the formation of a glial scar. They can ...
Neuron cell death is responsible for gliosis and results in the mushroom appearance of areas and is characteristic of ulegyria ... Normally an MRI of an ulegyria affected region will reveal groups of deteriorated neurons with gliosis present. In addition, ... For instance, ulegyria affected neurons experience gliosis in which glial cells, specifically astrocytes, build up near and ...
Mesial temporal sclerosis is a specific pattern of hippocampal neuronal loss accompanied by hippocampal gliosis and atrophy. ...
2003). "Expression and regulation of voltage-gated sodium channel beta1 subunit protein in human gliosis-associated pathologies ...
Retinal damage in mammals instead typically results in gliosis and scar formation which interrupts normal retinal function. ...
In such cases, gliosis may also be reversible. In all instances of gliosis resulting from CNS trauma, the long-term clinical ... but the extent and nature of the gliosis response vary widely based on the triggering insult. Gliosis in any form entails an ... Gliosis is the universal response of the CNS to tissue injury and occurs as a result of many acute conditions such as trauma, ... In this light, gliosis may be seen not only as a characteristic of many neuropathologies but as a potential contributor to, or ...
Gliosis: A process leading to scars in the central nervous system that involves the production of a dense fibrous network of ... Gliosis is a prominent feature of many diseases of the central nervous system, including multiple sclerosis and stroke. After a ...
Cite this page: Pernick N. Nodular & massive retinal gliosis. PathologyOutlines.com website. https://www.pathologyoutlines.com/ ...
Accumulated preclinical literature demonstrates that hypothalamic inflammation and gliosis are underlying causal components of ... The Significance of Hypothalamic Inflammation and Gliosis for the Pathogenesis of Obesity in Humans Endocr Rev. 2023 Mar 4;44(2 ... Both support the presence of hypothalamic inflammation and gliosis in children and adults with obesity. Findings predominantly ... Moreover, the severity of hypothalamic inflammation and gliosis has been related to comorbid conditions, including glucose ...
eNeuro eISSN: 2373-2822. The ideas and opinions expressed in eNeuro do not necessarily reflect those of SfN or the eNeuro Editorial Board. Publication of an advertisement or other product mention in eNeuro should not be construed as an endorsement of the manufacturers claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in eNeuro.. ...
Gliosis. Gliosis is identified in many pathologic specimens following surgical resection for frontal lobe epilepsy. It may ... gliosis, vascular malformations), neoplasms, head trauma, infections, and anoxia. ...
OIR mice showed increased gliosis. To determine the time course and duration of gliosis in the OIR retina, GFAP staining was ... Immunohistochemistry showed increased gliosis, microglial activation, and apoptosis with increasing age from P19 to P47. The ... An increase in GFAP signals indicating Müller cell gliosis and reactive astrocytes was observed as the OIR mice aged. For the ... Assessment of gliosis. Immunohistochemical staining for glial fibrillary acidic protein (GFAP; Thermo Fisher Scientific, ...
Assessment of gliosis around moveable implants in the brain. / Stice, Paula; Muthuswamy, Jitendran. In: Journal of neural ... Assessment of gliosis around moveable implants in the brain. In: Journal of neural engineering. 2009 ; Vol. 6, No. 4. ... Assessment of gliosis around moveable implants in the brain. Journal of neural engineering. 2009;6(4):046004. doi: 10.1088/1741 ... Stice, P., & Muthuswamy, J. (2009). Assessment of gliosis around moveable implants in the brain. Journal of neural engineering ...
Dive into the research topics of Reactive nonproliferative gliosis predominates in a chronic mouse model of glaucoma. ...
4 SomArchon expression in vivo does not cause gliosis.. SomArchon was expressed in the mouse brain by AAV2.9-Syn-SomArchon-P2A- ... suggesting that expression of SomArchon did not cause gliosis. Scale bars, 1 mm (a), 250 µm (b, c). ...
PET scans suggest gliosis may accompany persistent neurocognitive symptoms ... An index of gliosis was linked with persistent neurocognitive symptoms after mild or moderate SARS-CoV-2 infection, a small ... PET scans suggest gliosis may accompany persistent neurocognitive symptoms. by Judy George, Deputy Managing Editor, MedPage ... The study is the first to assess brain gliosis in long COVID, also known as post-acute sequelae of SARS-CoV-2 infection, Meyer ...
Stroke Subtype Dependent Synapse Elimination by Reactive Gliosis ... 1. Effect of gliosis on CNS injury. *Phagocytosis of glia cells ...
MIB1 in gliomas and gliosis Skjulsvik AJ, Torp SH [Volltext] Meeting Abstract (16dgnnP52) Cytotoxic effects of 4- ...
1994) Reactive gliosis as a consequence of interleukin-6 expression in the brain: studies in transgenic mice. Dev Neurosci 16: ... The severity of gliosis is diminished in GFAP-IL6/sgp130 mice. The development of reactive astrocytosis and microgliosis is ... IL-6 trans-signaling contributed to the development of gliosis in the cerebellum of GFAP-IL6 mice. A, Paraformaldehyde fixed, ... We therefore examined the degree of gliosis in the cerebellum of the GFAP-IL6 versus GFAP-IL6/sgp130 mice by GFAP (astrocyte ...
Gliosis. Moderate. Moderate. Minimal. Trachea. Lymphocytic tracheitis. Minimal. Minimal. Minimal. Lung. Interstitial pneumonia ...
Motor dysfunction and gliosis with preserved dopaminergic markers in human α-synuclein A30P transgenic mice. Neurobiology of ... Motor dysfunction and gliosis with preserved dopaminergic markers in human α-synuclein A30P transgenic mice. In: Neurobiology ... Motor dysfunction and gliosis with preserved dopaminergic markers in human α-synuclein A30P transgenic mice. / Gomez-Isla, ... Motor dysfunction and gliosis with preserved dopaminergic markers in human α-synuclein A30P transgenic mice. ...
Reactive gliosis as a consequence of interleukin-6 expression in the brain: studies in transgenic mice.. Chiang CS, Stalder A, ... The impact of microglia-derived cytokines upon gliosis in the CNS.. Giulian D, Li J, Li X, George J, Rutecki PA., Dev. Neurosci ... interleukin-6 application in vivo via macroencapsulation of interleukin-6-expressing COS-7 cells induces massive gliosis.. ... interleukin-6 application in vivo via macroencapsulation of interleukin-6-expressing COS-7 cells induces massive gliosis. Glia ...
Near infrared Raman spectroscopic study of reactive gliosis and the glial scar in injured rat spinal cords. / Saxena, Tarun; ... Near infrared Raman spectroscopic study of reactive gliosis and the glial scar in injured rat spinal cords. In XXII ... Near infrared Raman spectroscopic study of reactive gliosis and the glial scar in injured rat spinal cords. XXII International ... title = "Near infrared Raman spectroscopic study of reactive gliosis and the glial scar in injured rat spinal cords", ...
08.01.17Advanced Materials Injection of Microporous Annealing Particle (MAP) Hydrogels in the Stroke Cavity Reduces Gliosis and ... Hydrogels in the Stroke Cavity Reduces Gliosis and Inflammation and Promotes NPC Migration to the Lesion. Advanced Materials. ...
Astrocyte-specific expression of survivin after intracerebral hemorrhage in mice: A possible role in reactive gliosis? Journal ... Astrocyte-specific expression of survivin after intracerebral hemorrhage in mice: A possible role in reactive gliosis? / ... Astrocyte-specific expression of survivin after intracerebral hemorrhage in mice: A possible role in reactive gliosis?. ... title = "Astrocyte-specific expression of survivin after intracerebral hemorrhage in mice: A possible role in reactive gliosis ...
Because Müller cell gliosis is an important feature of early DR, the control of excessive gliosis may be a useful therapeutic ... reactive gliosis marker in DR [11,32]. Furthermore, Müller cell gliosis may impair neural-vascular relationships and contribute ... Reduction of reactive gliosis by E4 treatment in vivo and in vitro. The expression of GFAP in the retinas of 16-week-old GK ... and reducing reactive gliosis Yichao Fan,1 Kun Liu,2 Qingping Wang,1 Yuanyuan Ruan,3,4 Yu Zhang,1 Wen Ye1 ...
... this injury is accompanied by gliosis. Transient forebrain ischemia leads to delayed death of the CA1 neurons in the ...
... and so-called subcortical gliosis (Victoroff et al., 1994). ...
2008). Origin and progeny of reactive gliosis: a source of multipotent cells in the injured brain. Proc. Natl. Acad. Sci. U.S.A ... Robel, S., Berninger, B., and Gotz, M. (2011). The stem cell potential of glia: lessons from reactive gliosis. Nat. Rev. ... Pekny, M., and Nilsson, M. (2005). Astrocyte activation and reactive gliosis. Glia 50, 427-434. doi: 10.1002/glia.20207 ... mammalian astrocytes cease to produce neurons but rather undergo reactive gliosis, where they amplify themselves and form a ...
Newborn mice, ic: choroiditis, gliosis, vasculitis, perivasculitis with lymphocytic infiltration. Thymectomy abolished response ...
Overexpression of tau kinase cdk5 activator p25 resulted in gliosis. As astroglia and microglia fuelled inflammation, rapid ...
gliosis, a type of scarring in the brain Musicogenic epilepsy has been linked to activity in the temporal lobe. on the non- ...
... originates primarily from slow neuronal degeneration consequently resulting in lesser extent of concomitant reactive gliosis in ... The intensity and extent of the reactive gliosis are determined primarily by signals from damaged cells (e.g., [56, 57]). Up to ... In grade 1, neuronal loss is accompanied by reactive gliosis, which is evident primarily in the head and tail, less in the body ... A. Buffo, I. Rite, P. Tripathi et al., "Origin and progeny of reactive gliosis: a source of multipotent cells in the injured ...
  • Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). (wikipedia.org)
  • citation needed] Reactive astrogliosis is the most common form of gliosis and involves the proliferation of astrocytes, a type of glial cell responsible for maintaining extracellular ion and neurotransmitter concentrations, modulating synapse function, and forming the blood-brain barrier. (wikipedia.org)
  • Astrocyte-specific expression of survivin after intracerebral hemorrhage in mice: A possible role in reactive gliosis? (elsevierpure.com)
  • The expressions of retinal GLP-1R, mitochondria-dependent apoptosis-associated genes, reactive gliosis markers, and endoplasmic reticulum stress-related pathway genes were studied by western blotting and immunohistochemistry in vivo and in vitro. (molvis.org)
  • It also downregulated the expression of glial fibrillary acidic protein and reduced retinal reactive gliosis. (molvis.org)
  • E4 may protect retinal cells from diabetic attacks by activating GLP-1R, decreasing retinal cell apoptosis, and reducing retinal reactive gliosis. (molvis.org)
  • A basic difference between HD pathology in human and tgHD51 rats is in the rate of NDP progression that originates primarily from slow neuronal degeneration consequently resulting in lesser extent of concomitant reactive gliosis in the brain of tgHD51 rats. (hindawi.com)
  • Regardless of the development of reactive gliosis within the striatum, loss of the grey matter is extensive and results in the compensatory enlargement of lateral brain ventricles. (hindawi.com)
  • In grade 1, neuronal loss is accompanied by reactive gliosis, which is evident primarily in the head and tail, less in the body of CN. (hindawi.com)
  • Is reactive gliosis a property of a distinct subpopulation of astrocytes? (jneurosci.org)
  • Reactive gliosis and microglial reaction decreased in the same groups (AX+FS, AX+CFS) at 4 weeks. (hindawi.com)
  • Heterogeneous group of neurodegenerative disorders characterized by frontal and temporal lobe atrophy associated with neuronal loss, gliosis, and dementia. (bvsalud.org)
  • AD is characterized grossly by progressive atrophy and gliosis, first of the hippocampus and medial temporal lobe, followed by other association cortices (frontal and parietal lobes), and finally by primary motor or sensory cortex (occipital lobe). (medscape.com)
  • Other causes included congenital pathology, calcifications, atrophy and gliosis. (ajol.info)
  • Immunohistochemistry showed increased gliosis, microglial activation, and apoptosis with increasing age from P19 to P47. (molvis.org)
  • For both newborns, significant histopathologic changes were limited to the brain, and included parenchymal calcification, microglial nodules, gliosis, and cell degeneration and necrosis. (cdc.gov)
  • In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes. (wikipedia.org)
  • However, there is limited understanding of the molecular underpinnings associated with toxicant- or occupational injury-mediated neuroinflammation, gliosis, and neurological outcomes. (cdc.gov)
  • Accumulated preclinical literature demonstrates that hypothalamic inflammation and gliosis are underlying causal components of diet-induced obesity in rodent models. (nih.gov)
  • Both support the presence of hypothalamic inflammation and gliosis in children and adults with obesity. (nih.gov)
  • Moreover, the severity of hypothalamic inflammation and gliosis has been related to comorbid conditions, including glucose intolerance, insulin resistance, type 2 diabetes, and low testosterone levels in men, independent of elevated body adiposity. (nih.gov)
  • Cross-sectional findings are augmented by a small number of prospective studies suggesting that a greater degree of hypothalamic inflammation and gliosis may predict adiposity gain and worsening insulin sensitivity in susceptible individuals. (nih.gov)
  • Like other forms of gliosis, astrogliosis accompanies traumatic brain injury as well as many neuropathologies, ranging from amyotrophic lateral sclerosis to fatal familial insomnia. (wikipedia.org)
  • Stice, P & Muthuswamy, J 2009, ' Assessment of gliosis around moveable implants in the brain ', Journal of neural engineering , vol. 6, no. 4, 046004. (elsevierpure.com)
  • The study is the first to assess brain gliosis in long COVID, also known as post-acute sequelae of SARS-CoV-2 infection, Meyer and co-authors said. (medpagetoday.com)
  • Blockade of trans-signaling in the brain of the GFAP-IL6 mice significantly attenuated Serpina3n but not SOCS3 gene expression, whereas vascular changes including angiogenesis and blood-brain barrier leakage as well as gliosis were also reduced significantly. (jneurosci.org)
  • Extensive fetal brain parenchymal injury/gliosis, >10% of supratentorial brain volume (i.e. (childrenshospital.org)
  • After a stroke, neurons die and disappear with replacement gliosis. (rxlist.com)
  • We demonstrated histological evidence of persistent ectopic synapses, prolonged cellular apoptosis, and gliosis in the OIR retina that corresponded with long-term in vivo evidence of capillary attrition, inner retinal thinning, and dysfunction despite full peripheral revascularization. (molvis.org)
  • The final component of gliosis is astrogliosis, the proliferation of surrounding astrocytes, which are the main constituents of the glial scar. (wikipedia.org)
  • The changes are confined to cerebral white matter and suggest an accumulation of lipids, periventricular gliosis, delayed myelination, and a mild permanent myelin deficit. (ajnr.org)
  • Accompanying pathologic changes include gliosis and characteristic histologic vacuolar (spongiform) changes, resulting in dementia and other neurologic deficits. (msdmanuals.com)
  • Continuous interleukin-6 application in vivo via macroencapsulation of interleukin-6-expressing COS-7 cells induces massive gliosis. (uni-bielefeld.de)
  • An index of gliosis was linked with persistent neurocognitive symptoms after mild or moderate SARS-CoV-2 infection, a small case-control study showed. (medpagetoday.com)
  • On Magnetic Resonance Imaging (MRI), gliosis with ill-defined FLAIR hyperintense signal was seen in the left periventricular white matter and corona radiata with ex vacuo dilatation of left lateral ventricle. (eurorad.org)
  • The process of gliosis involves a series of cellular and molecular events that occur over several days. (wikipedia.org)
  • This review highlights the research focusing on the direct interaction between the immune system and the toxicant- or occupational injury-induced gliosis. (cdc.gov)
  • This process, which constitutes a form of gliosis known as microgliosis, begins within hours of the initial CNS injury. (wikipedia.org)
  • this injury is accompanied by gliosis. (nih.gov)
  • However, gliosis has been shown to have both beneficial and detrimental effects, and the balance between these is due to a complex array of factors and molecular signaling mechanisms, which affect the reaction of all glial cell types. (wikipedia.org)
  • Histological analysis of this line showed aberrant expression of the protein in cell soma and progressive CNS gliosis, but no discrete Lewy body-like α-synuclein inclusions could be identified. (umn.edu)
  • In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar. (wikipedia.org)
  • Gliosis is a prominent feature of many diseases of the central nervous system, including multiple sclerosis and stroke . (rxlist.com)
  • A number of post-mortem reports on epileptics, as reviewed by Meldrum, Horton, and Brierley (1974) have indicated neuronal loss and gliosis, especially in the hippocampus and temporal lobe. (healthyplace.com)
  • Studies of post-mortem brains of HIV/AIDS patients who suffer from HAND have shown neural circuitry atrophy, with neuronal loss and gliosis, especially in hippocampal and forebrain cortical areas. (nih.gov)
  • Term neonates had significant cortical and subcortical gliosis and atrophy in the parasagittal watershed areas. (ajnr.org)
  • Molecular imaging of retinal gliosis in transgenic mice induced by kainic acid neurotoxicity. (nih.gov)
  • The present study aimed to examine the possible role of astrocyte-derived S100B in the progression of cerebral amyloidosis and gliosis in transgenic mice overproducing mutant amyloid precursor protein (Tg APPsw mice, line 2576). (nih.gov)
  • Retinal gliosis can occur as a primary change (generally of uncertain etiology) or as a feature to other retinal lesions (e.g., degeneration). (nih.gov)
  • When occurring as a primary change, retinal gliosis should be diagnosed and assigned a severity grade. (nih.gov)
  • Like other forms of gliosis, astrogliosis accompanies traumatic brain injury as well as many neuropathologies, ranging from amyotrophic lateral sclerosis to fatal familial insomnia. (wikipedia.org)
  • In conclusion, a clinically comparable dose of MgSO4 was associated with moderate improvements in white and grey matter gliosis and myelin density but did not improve EEG maturation or neuronal or oligodendrocyte survival . (bvsalud.org)
  • This process, which constitutes a form of gliosis known as microgliosis, begins within hours of the initial CNS injury. (wikipedia.org)
  • In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar. (wikipedia.org)
  • Gliosis has historically been given a negative connotation due to its appearance in many CNS diseases and the inhibition of axonal regeneration caused by glial scar formation. (wikipedia.org)
  • However, gliosis has been shown to have both beneficial and detrimental effects, and the balance between these is due to a complex array of factors and molecular signaling mechanisms, which affect the reaction of all glial cell types. (wikipedia.org)
  • The 36-week neonate had mild cortical and subcortical atrophy and gliosis superimposed on deep white matter and periventricular gliosis. (ajnr.org)
  • Postterm neonates (44-46 weeks) showed cortical and subcortical watershed gliosis and atrophy with sparing of the immediate periventricular region. (ajnr.org)
  • 23. Gliosis versus glioma? (nih.gov)
  • 28. Receptor tyrosine kinase expression in astrocytic lesions: similar features in gliosis and glioma. (nih.gov)
  • Areas of inflammation, axonal loss, demyelination and gliosis, occurring throughout the brain and spinal cord, are the distinctive features of Multiple Sclerosis (MS). (biorxiv.org)
  • Histology shows persistent ectopic synapses, neuronal apoptosis, and gliosis in RA and OIR mice. (rochester.edu)
  • Status of the presence of gliosis. (nih.gov)
  • The presence of gliosis in the hypocretin cell region is consistent with a degenerative process being the cause of the Hcrt cell loss in narcolepsy. (ucla.edu)
  • Magnesium sulphate reduces tertiary gliosis but does not improve EEG recovery or white or grey matter cell survival after asphyxia in preterm fetal sheep. (bvsalud.org)
  • The analysis demonstrated that gossypetin prevented the expression of genes associated with gliosis *2 , which promotes chronic inflammatory reactions, while increasing the expression of genes associated with Aβ phagocytosis. (postech.ac.kr)
  • The process of gliosis involves a series of cellular and molecular events that occur over several days. (wikipedia.org)
  • Patients at 24- and 26-weeks gestational age had irregularly enlarged ventricular trigones with minimal periventricular gliosis. (ajnr.org)
  • By using the amygdala (AMY) and white matter (WM) as reference regions, MBH:AMY and MBH:WM T2 signal ratios were calculated as a radiologic measure of MBH gliosis. (figshare.com)
  • Linear regressions examined associations between GDM exposure (GDM overall, and by timing of GDM exposure ( £ 26 weeks or >26 weeks) and MBH gliosis. (figshare.com)
  • Patients at 28-34 weeks had variably dilated ventricles with periventricular gliosis. (ajnr.org)