Copper chelator that inhibits monoamine oxidase and causes liver and brain damage.
Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.
Broad plate of dense myelinated fibers that reciprocally interconnect regions of the cortex in all lobes with corresponding regions of the opposite hemisphere. The corpus callosum is located deep in the longitudinal fissure.
The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.
A class of large neuroglial (macroglial) cells in the central nervous system. Oligodendroglia may be called interfascicular, perivascular, or perineuronal (not the same as SATELLITE CELLS, PERINEURONAL of GANGLIA) according to their location. They form the insulating MYELIN SHEATH of axons in the central nervous system.
A 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)
Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS.
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.
An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.
The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.
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.

Insulin-like growth factor-1 inhibits mature oligodendrocyte apoptosis during primary demyelination. (1/102)

Metabolic insult results in apoptosis and depletion of mature oligodendrocytes during demyelination. To examine the role of insulin-like growth factor-1 (IGF-1) during acute demyelination and remyelination in the adult CNS, we exposed transgenic mice that continuously express IGF-1 (IGF-1 tg) to cuprizone intoxication. Demyelination was observed within the corpus callosum in both wild-type and IGF-1 tg mice 3 weeks after exposure to cuprizone. Wild-type mice showed significant apoptotic mature oligodendrocytes and a dramatic loss of these cells within the lesion that resulted in near complete depletion and demyelination by week 5. In contrast, the demyelinated corpus callosum of the IGF-1 tg mice was near full recovery by week 5. This rapid recovery was apparently caused by survival of the mature oligodendrocyte population because apoptosis was negligible, and by week 4, the mature oligodendrocyte population was completely restored. Furthermore, despite demyelination in both wild-type and IGF-1 tg mice, oligodendrocyte progenitors accumulated only in the absence of mature oligodendrocytes and failed to accumulate if the mature oligodendrocytes remained as demonstrated in the IGF-1 tg mice. These results suggest that IGF-1 may be important in preventing the depletion of mature oligodendrocytes in vivo and thus facilitates an early recovery from demyelination.  (+info)

Absence of macrophage-inflammatory protein-1alpha delays central nervous system demyelination in the presence of an intact blood-brain barrier. (2/102)

Chemokines are small chemotactic cytokines that modulate leukocyte recruitment and activation during inflammation. Here, we describe the role of macrophage inflammatory protein-1alpha (MIP-1alpha) during cuprizone intoxication, a model where demyelination of the CNS features a large accumulation of microglia/macrophage without T cell involvement or blood-brain barrier disruption. RNase protection assays showed that mRNA for numerous chemokines were up-regulated during cuprizone treatment in wild-type, C57BL/6 mice. RANTES, inflammatory protein-10, and monocyte chemoattractant protein-1 showed greatest expression with initiation of insult at 1-2 wk of treatment, whereas MIP-1alpha and beta increased later at 4-5 wk, coincident with peak demyelination and cellular accumulation. The function of MIP-1alpha during demyelination was tested in vivo by exposing MIP-1alpha knockout mice (MIP-1alpha(-/-)) to cuprizone and comparing pathology to wild-type mice. Demyelination at 3.5 wk of treatment was significantly decreased in MIP-1alpha(-/-) mice ( approximately 36% reduction), a result confirmed by morphology at the electron microscopic level. The delay in demyelination was correlated to apparent decreases in microglia/macrophage and astrocyte accumulation and in TNF-alpha protein levels. It was possible that larger effects of the MIP-1alpha deficiency were being masked by other redundant chemokines. Indeed, RNase protection assays revealed increased expression of several chemokine transcripts in both untreated and cuprizone-treated MIP-1alpha(-/-) mice. Nonetheless, despite this possible compensation, our studies show the importance of MIP-1alpha in demyelination in the CNS and highlight its effect, particularly on cellular recruitment and cytokine regulation.  (+info)

Interleukin-1beta promotes repair of the CNS. (3/102)

Interleukin-1beta (IL-1beta) is a proinflammatory cytokine associated with the pathophysiology of demyelinating disorders such as multiple sclerosis and viral infections of the CNS. However, we demonstrate here that IL-1beta appears to promote remyelination in the adult CNS. In IL-1beta(-/-) mice, acute demyelination progressed similarly to wild-type mice and showed parallel mature oligodendrocyte depletion, microglia-macrophage accumulation, and the appearance of oligodendrocyte precursors. In contrast, IL-1beta(-/-) mice failed to remyelinate properly, and this appeared to correlate with a lack of insulin-like growth factor-1 (IGF-1) production by microglia-macrophages and astrocytes and to a profound delay of precursors to differentiate into mature oligodendrocytes. Thus, IL-1beta may be crucial to the repair of the CNS, presumably through the induction of astrocyte and microglia-macrophage-derived IGF-1.  (+info)

The protective role of nitric oxide in a neurotoxicant-induced demyelinating model. (4/102)

Demyelination is often associated with acute inflammatory events involving the recruitment-activation of microglia/macrophage, astrocytes, and leukocytes. The ultimate role of inflammatory products in demyelinating disease and in the survival of oligodendrocytes, the myelin forming cells, is unresolved. The current study examines the role of inducible NO synthase (iNOS)-derived NO in a neurotoxicant-induced model of demyelination. NO levels were greatly elevated in the midline corpus callosum during demyelination in genetically intact C57BL/6 mice, and this NO was due solely to the induction of iNOS, as the correlates of NO were not found in mice lacking iNOS. C57BL/6 mice lacking iNOS exhibited more demyelination, but did not display an increased overall cellularity in the corpus callosum, attributable to an unimpeded microglia/macrophage presence. An enhanced course of pathology was noted in mice lacking iNOS. This was associated with a greater depletion of mature oligodendrocytes, most likely due to apoptosis of oligodendrocytes. Microglia and astrocytes did not undergo apoptosis during treatment. Our results suggest a moderately protective role for NO during acute inflammation-association demyelination.  (+info)

Absence of fibroblast growth factor 2 promotes oligodendroglial repopulation of demyelinated white matter. (5/102)

This study takes advantage of fibroblast growth factor 2 (FGF2) knock-out mice to determine the contribution of FGF2 to the regeneration of oligodendrocytes in the adult CNS. The role of FGF2 during spontaneous remyelination was examined using two complementary mouse models of experimental demyelination. The murine hepatitis virus strain A59 (MHV-A59) model produces focal areas of spinal cord demyelination with inflammation. The cuprizone neurotoxicant model causes extensive corpus callosum demyelination without a lymphocytic cell response. In both models, FGF2 expression is upregulated in areas of demyelination in wild-type mice. Surprisingly, in both models, oligodendrocyte repopulation of demyelinated white matter was significantly increased in FGF2 -/- mice compared with wild-type mice and even surpassed the oligodendrocyte density of nonlesioned mice. This dramatic result indicated that the absence of FGF2 promoted oligodendrocyte regeneration, possibly by enhancing oligodendrocyte progenitor proliferation and/or differentiation. FGF2 -/- and +/+ mice had similar oligodendrocyte progenitor densities in normal adult CNS, as well as similar progenitor proliferation and accumulation during demyelination. To directly analyze progenitor differentiation, glial cultures from spinal cords of wild-type mice undergoing remyelination after MHV-A59 demyelination were treated for 3 d with either exogenous FGF2 or an FGF2 neutralizing antibody. Elevating FGF2 favored progenitor proliferation, whereas attenuating endogenous FGF2 activity promoted the differentiation of progenitors into oligodendrocytes. These in vitro results are consistent with enhanced progenitor differentiation in FGF2 -/- mice. These studies demonstrate that the FGF2 genotype regulates oligodendrocyte regeneration and that FGF2 appears to inhibit oligodendrocyte lineage differentiation during remyelination.  (+info)

Insulin-like growth factor (IGF) signaling through type 1 IGF receptor plays an important role in remyelination. (6/102)

We examined the role of IGF signaling in the remyelination process by disrupting the gene encoding the type 1 IGF receptor (IGF1R) specifically in the mouse brain by Cre-mediated recombination and then exposing these mutants and normal siblings to cuprizone. This neurotoxicant induces a demyelinating lesion in the corpus callosum that is reversible on termination of the insult. Acute demyelination and oligodendrocyte depletion were the same in mutants and controls, but the mutants did not remyelinate adequately. We observed that oligodendrocyte progenitors did not accumulate, proliferate, or survive within the mutant mice, compared with wild type, indicating that signaling through the IGF1R plays a critical role in remyelination via effects on oligodendrocyte progenitors.  (+info)

Insulin-like growth factor I gene expression is induced in astrocytes during experimental demyelination. (7/102)

To investigate insulin-like growth factor I (IGF-I) and IGF-I receptor gene expression during experimental demyelination and myelin regeneration, young mice were fed cuprizone (( bis(cyclohexanone) oxaldihydrazone )). This copper-chelating agent produces demyelination in the corpus callosum and superior cerebellar peduncles, and when treatment is stopped, there is rapid remyelination. At intervals during cuprizone treatment and recovery, brain sections were hybridized with specific probes and immunostained with antibodies to determine the localization and relative amounts of IGF-I and IGF-I receptor mRNAs and peptides. In untreated littermates, IGF-I and IGF-I receptor mRNAs and peptides were not detected in white matter. In cuprizone-treated mice, high levels of both IGF-I mRNA and peptide were expressed by astrocytes in areas of myelin breakdown. Astrocyte IGF-I expression decreased rapidly during recovery and oligodendroglial expression of myelin-related genes increased. In severely demyelinated areas, immature oligodendroglia exhibited a transient increase in IGF-I receptor mRNA and peptide immunoreactivity during early recovery. This highly specific pattern of IGF-I induction in astrocytes during demyelination and the expression of the IGF-I receptor in regenerating oligodendrocytes during recovery suggest that IGF-I functions in the regulation of oligodendrocyte and myelin metabolism in vivo.  (+info)

Functional genomic analysis of remyelination reveals importance of inflammation in oligodendrocyte regeneration. (8/102)

Tumor necrosis factor alpha (TNFalpha), a proinflammatory cytokine, was shown previously to promote remyelination and oligodendrocyte precursor proliferation in a murine model for demyelination and remyelination. We used Affymetrix microarrays in this study to identify (1) changes in gene expression that accompany demyelination versus remyelination and (2) changes in gene expression during the successful remyelination of wild-type mice versus the unsuccessful attempts in mice lacking TNFalpha. Alterations in inflammatory genes represented the most prominent changes, with major histocompatibility complex (MHC) genes dramatically enhanced in microglia and astrocytes during demyelination, remyelination, and as a consequence of TNFalpha stimulation. Studies to examine the roles of these genes in remyelination were then performed using mice lacking specific genes identified by the microarray. Analysis of MHC-II-null mice showed delayed remyelination and regeneration of oligodendrocytes, whereas removal of MHC-I had little effect. These data point to the induction of MHC-II by TNFalpha as an important regulatory event in remyelination and emphasize the active inflammatory response in regeneration after pathology in the brain.  (+info)

The most common demyelinating diseases include:

1. Multiple sclerosis (MS): An autoimmune disease that affects the CNS, including the brain, spinal cord, and optic nerves. MS causes inflammation and damage to the myelin sheath, leading to a range of symptoms such as muscle weakness, vision problems, and cognitive difficulties.
2. Acute demyelination: A sudden, severe loss of myelin that can be caused by infections, autoimmune disorders, or other factors. This condition can result in temporary or permanent nerve damage.
3. Chronic inflammatory demyelination (CIDP): A rare autoimmune disorder that causes progressive damage to the myelin sheath over time. CIDP can affect the CNS and the peripheral nervous system (PNS).
4. Moore's disease: A rare genetic disorder that results in progressive demyelination of the CNS, leading to a range of neurological symptoms including muscle weakness, seizures, and cognitive difficulties.
5. Leukodystrophies: A group of genetic disorders that affect the development or function of myelin-producing cells in the CNS. These conditions can cause progressive loss of myelin and result in a range of neurological symptoms.

Demyelinating diseases can be challenging to diagnose, as the symptoms can be similar to other conditions and the disease progression can be unpredictable. Treatment options vary depending on the specific condition and its severity, and may include medications to reduce inflammation and modulate the immune system, as well as rehabilitation therapies to help manage symptoms and improve quality of life.

Gliosis is made up of glial cells, which are non-neuronal cells that provide support and protection to neurons. When neural tissue is damaged, glial cells proliferate and form a scar-like tissue to fill in the gap and repair the damage. This scar tissue can be made up of astrocytes, oligodendrocytes, or microglia, depending on the type of injury and the location of the damage.

Gliosis can have both beneficial and harmful effects on the brain. On one hand, it can help to prevent further damage by providing a physical barrier against invading substances and protecting the surrounding neural tissue. It can also promote healing by bringing in immune cells and growth factors that aid in the repair process.

On the other hand, gliosis can also have negative effects on brain function. The scar tissue can disrupt normal communication between neurons, leading to impaired cognitive and motor function. In addition, if the scar tissue is too extensive or severe, it can compress or displaces surrounding neural tissue, leading to long-term neurological deficits or even death.

There are several ways to diagnose gliosis, including magnetic resonance imaging (MRI), positron emission tomography (PET), and histopathology. Treatment options for gliosis depend on the underlying cause of the condition and can include medications, surgery, or a combination of both.

In summary, gliosis is a type of scar tissue that forms in the brain and spinal cord as a result of damage to neural tissue. It can have both beneficial and harmful effects on brain function, and diagnosis and treatment options vary depending on the underlying cause of the condition.

Silverstroff, L.; Batucci, S.; Pasquini, J.; Franco, P. (2012). "Cuprizone-induced demyelination in the rat cerebral cortex and ... "The cyclooxygenase-2 pathway via the pge₂ ep2 receptor contributes to oligodendrocytes apoptosis in cuprizone-induced ...
"Cerebroside synthesis as a measure of the rate of remyelination following cuprizone-induced demyelination in brain". Journal of ...
... the resolution of status spongiosus and remyelination in cuprizone intoxication in mice". J. Neurocytol. 1 (4): 413-26. doi: ...
"Cerebroside synthesis as a measure of the rate of remyelination following cuprizone-induced demyelination in brain". Journal of ...
Moreover, it improved memorizing abilities in rats after i.p. administration and restored the myelin loss in cuprizone-induced ... "The novel synthetic microneurotrophin BNN27 protects mature oligodendrocytes against cuprizone-induced death, through the NGF ...
... lacking mice also exhibit a different regulation of this protein after oligodendrocyte damage induced by the chemical cuprizone ...
Elevated expression of GPR84 was also observed during the demyelination phase of the reversible Cuprizone-Induced Demyelinating ...
Effects of Kolaviron on Behavioural Deficits and Oxidative Damage in Prefrontal Cortex and Hippocampus of Cuprizone-Induced ...
Toxic exposures to methionine sulfoxime, cuprizone, isoniazid, triethyl tin, hexachlorophene, and hydrogen cyanide have been ...
... in response to demyelination in acute or chronic lesions created by chemical agents such as lysolecithin or cuprizone, and ...
... cuprizone MeSH D02.455.426.392.368.367.204 - cyclamates MeSH D02.455.426.392.368.367.218 - cyclohexanecarboxylic acids MeSH ...
Cuprizone. Known as: Oxaldihydrazone, Biscyclohexanone, Cuprizone [Chemical/Ingredient], Ethanedioic acid, bis( ... Gene Expression in Brain during Cuprizone-Induced Demyelination and Remyelination. *P. Morell, C. Barrett, +4 authors. G. ... The cuprizone model of toxic demyelination in the central nervous system is commonly used to investigate the pathobiology of… ... The Neurotoxicant, Cuprizone, as a Model to Study Demyelination and Remyelination in the Central Nervous System ...
... and remyelination in cuprizone-treated mice. NMR Biomed, 28(3), 327-337. doi:10.1002/nbm.3253. ... Deep gray matter demyelination detected by magnetization transfer ratio in the cuprizone model. PLoS One, 8(12), e84162. doi: ... Quantitative MRI and ultrastructural examination of the cuprizone mouse model of demyelination. NMR Biomed, 26(11), 1562-1581. ... MRI identification of the rostral-caudal pattern of pathology within the corpus callosum in the cuprizone mouse model. J Magn ...
... cuprizone-induced multiple sclerosis-like pathology, insulin overdose, or magnesium overdose (Sikiric et al., 2013; Medvidovic- ...
... after NSAIDs or insulin overdose or cuprizone encephalopathies were attenuated along with GI, liver and vascular injuries. ... after NSAIDs or insulin overdose or cuprizone encephalopathies were attenuated along with GI, liver and vascular injuries. ...
Cuprizone (CPZ) model is a toxic demyelination model. The purpose of this study was to develop an MS model by cuprizone ... Cuprizone-induced demyelination in Wistar rats; electrophysiological and histological assessment. Basoglu, H; Boylu, N T; Kose ... These results indicated that 6 weeks of cuprizone feedings could be suitable to bring into existence of MS model in Wistar rats ... CONCLUSIONS: SNCV of the rats were feed with cuprizone began tendency of decrease after 4th weeks. These reductions were ...
Cuprizone model: grip test, ledged beam test, and myelin staining. IN VIVO PHARMACOLOGY CATALOG , MS. NEU-A04-1. Multiple ...
Cuprizone - Preferred Concept UI. M0005418. Scope note. Copper chelator that inhibits monoamine oxidase and causes liver and ...
... microscopy showed cuprizone-induced demyelination in the corpus callosum and nearly complete remyelination after cuprizone ... microscopy showed cuprizone-induced demyelination in the corpus callosum and nearly complete remyelination after cuprizone ... microscopy showed cuprizone-induced demyelination in the corpus callosum and nearly complete remyelination after cuprizone ... microscopy showed cuprizone-induced demyelination in the corpus callosum and nearly complete remyelination after cuprizone ...
Journal Article] Prostaglandin F2α FP receptor inhibitor reduce demyelination and motor dysfunction in a cuprizone-induced ... Presentation] Prostaglandin F2α FP receptor inhibitor reduce demyelination and motor dysfunction in a cuprizone-induced ... Presentation] Prostaglandin F2α FP receptor inhibitor reduce demyelination and motor dysfunction in a cuprizone-induced ... Presentation] Prostaglandin F2α FP receptor inhibitor reduce demyelination and motor dysfunction in a cuprizone-induced ...
A cuprizone (CPZ) -induced schizophrenic mice model was established. Agomelatine, a MT1 and MT2 agonist, was administrated ... Notably, all these effects of agomelatine are markedly weakened by an autophagy inducer Rapamycin (RAPA). In vitro, cuprizone ... Importantly, agomelatine suppresses CDK5 expression and autophagic flux against cuprizone, which to the contrary is blocked by ... induced by cuprizone in CDK5-dependent manner, as well as reducing cellular apoptosis. ...
PubMed, Coenzyme Q10 enhances remyelination and regulate inflammation effects of cuprizone in corpus callosum of chronic model ...
Copper sulfide is naturally occurring in nature as a mineral, called cuprizone. It conducts electricity moderately. Both ...
The Cuprizone Mouse Model: A Comparative Study of Cuprizone Formulations from Different Manufacturers. ... In this study, we tested whether different Cuprizone formulations from different vendors and manufacturers influenced Cuprizone ... Cuprizone groups (n = 12 +12), sham groups (n = 4 +4), and carboxy-methyl-cellulose groups (n = 3 +3). Cuprizone-fed rats ... The Cuprizone mouse model is widely used in studies on de- and remyelination. In the hands of different experimenters, the ...
... cuprizone (CPZ) diet model, a toxic demyelination model. MSC-Exo or PBS were intravenously injected twice a week for 4 weeks, ...
Protective impacts of erythropoietin on myelinization of oligodendrocytes and schwann cells in CNS and PNS following cuprizone- ... Protective impacts of erythropoietin on myelinization of oligodendrocytes and schwann cells in CNS and PNS following cuprizone- ...
... but a trace of Dietary vitamin d3 supplements reduce demyelination in the cuprizone model The second floor of the Hall of ...
... the PPMS NPCs did not provide neuroprotection against demyelination in cuprizone-fed mice and did not support OPC ...
Stable gastric pentadecapeptide BPC 157 heals cysteamine-colitis and colon-colon-anastomosis and counteracts cuprizone brain ...
"Diffusion kurtosis imaging probes cortical alterations and white matter pathology following cuprizone-induced demyelination and ...
Cuprizone and EAE mouse frontal cortex proteomics revealed proteins altered in multiple sclerosis Eystein Oveland 1 , Intakhar ... Cuprizone and EAE mouse frontal cortex proteomics revealed proteins altered in multiple sclerosis Eystein Oveland et al. Sci ... The cuprizone model reflects de- and remyelination in multiple sclerosis, and the experimental autoimmune encephalomyelitis ( ... Legumain and C1Q complement proteins were among the most upregulated proteins in cuprizone and hemopexin in the EAE model. ...
Cuprizone demyelination induces a unique inflammatory response in the subventricular zone. January 22, 2016 ... Thalamocortical-auditory network alterations following cuprizone-induced demyelination. January 22, 2016 *[ MEDLINE Abstract ] ... oligodendrocyte loss and demyelination in the cuprizone mouse model. January 09, 2016 ...
In the present study, we used a murine model of cuprizone-induced demyelination to broaden the application of PBR as a marker ... Our findings indicate that brain PBR levels increased as a function of dose and duration of cuprizone treatment and it was ... C57BL/6J mice were maintained on a cuprizone-containing or control diet and sacrificed at specific time points after initiation ... MeSH Terms: Animals; Astrocytes/metabolism; Autoradiography/methods; Biomarkers/analysis; Cerebral Cortex/metabolism; Cuprizone ...
Neurobiological effects of sphingosine 1-phosphate receptor modulation in the cuprizone model.. Kim HJ, Miron VE, Dukala D, ...
9. CZ-7, a new derivative of Claulansine F, promotes remyelination induced by cuprizone by enhancing myelin debris clearance. ... Electroacupuncture Promotes Remyelination after Cuprizone Treatment by Enhancing Myelin Debris Clearance.. Zhu K; Sun J; Kang Z ... Fasudil enhances the phagocytosis of myelin debris and the expression of neurotrophic factors in cuprizone-induced ...
Myelin stained images from (A) a control mouse brain and (B) a cuprizone-treated mouse brain. The cuprizone-treated mouse brain ... Average frequency images and T2* maps in control and cuprizone-treated fixed mouse brains in vitro. In-vitro images also show ... Averaged frequency images and T2* maps in control and cuprizone-treated mice in vivo. Compared to the control (B and D), the ... Spatio-Temporal Patterns of Demyelination and Remyelination in the Cuprizone Mouse Model. Tagge I, OConnor A, Chaudhary P, ...
Cuprizone Preferred Term Term UI T010085. Date01/01/1999. LexicalTag NON. ThesaurusID ... Cuprizone Preferred Concept UI. M0005418. Registry Number. 5N16U7E0AO. Related Numbers. 370-81-0. Scope Note. Copper chelator ... Cuprizone. Tree Number(s). D02.455.426.392.368.367.190. Unique ID. D003471. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/ ...
Cuprizone Preferred Term Term UI T010085. Date01/01/1999. LexicalTag NON. ThesaurusID ... Cuprizone Preferred Concept UI. M0005418. Registry Number. 5N16U7E0AO. Related Numbers. 370-81-0. Scope Note. Copper chelator ... Cuprizone. Tree Number(s). D02.455.426.392.368.367.190. Unique ID. D003471. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/ ...
... equilibrium cyclohexadiene taeanensis neurosyphilis testosterones adjustor lrha sejugis unilateralis soricina camels cuprizone ...
... cuprizone (CPZ) diet model, a toxic demyelination model. MSC-Exo or PBS were intravenously injected twice a week for 4 weeks, ...
Cucurbitacins N0000170194 Cullin Proteins N0000006901 cupric chloride N0000179092 cupric oxide N0000166392 Cuprizone ...
AB - The membrane potentials and resistances of giant mitochondria from mice fed cuprizone have been studied. They were found ... AB - Single giant mitochondria isolated from mice fed cuprizone were assayed for their metabolic viability. Two tests were ...
CHELATING AGENTS CUPRIZONE CHELATING AGENTS DEFEROXAMINE CHELATING AGENTS DIMERCAPROL CHELATING AGENTS DITHIZONE CHELATING ... MONOAMINE OXIDASE INHIBITORS CUPRIZONE MONOAMINE OXIDASE INHIBITORS FURAZOLIDONE MONOAMINE OXIDASE INHIBITORS HARMINE MONOAMINE ... ENZYME INHIBITORS CUPRIZONE ENZYME INHIBITORS CURCUMIN ENZYME INHIBITORS CYCLOHEXIMIDE ENZYME INHIBITORS CYCLOOXYGENASE ...
  • 4. The Effect of Stereotactic Injections on Demyelination and Remyelination: a Study in the Cuprizone Model. (nih.gov)
  • 7. Demyelination and remyelination in anatomically distinct regions of the corpus callosum following cuprizone intoxication. (nih.gov)
  • 8. G protein-coupled receptor 30 contributes to improved remyelination after cuprizone-induced demyelination. (nih.gov)
  • 12. rHIgM22 enhances remyelination in the brain of the cuprizone mouse model of demyelination. (nih.gov)
  • 16. Quantitative temporal changes in DTI values coupled with histological properties in cuprizone-induced demyelination and remyelination. (nih.gov)
  • 18. Spatio-Temporal Patterns of Demyelination and Remyelination in the Cuprizone Mouse Model. (nih.gov)
  • Likewise, electron microscopy showed cuprizone-induced demyelination in the corpus callosum and nearly complete remyelination after cuprizone removal. (elsevierpure.com)
  • 8. ghaiad, H. R., M. M. Nooh, M. M. El-Sawalhi, and A. A. Shaheen, "Resveratrol Promotes Remyelination in Cuprizone Model of Multiple Sclerosis: Biochemical and Histological Study. (cu.edu.eg)
  • After a 4-week cuprizone diet, cuprizone was removed and PBS or rhGas6 (400 ng/ml, 4 μg/ml and 40 μg/ml) was delivered by osmotic mini-pump into the corpus callosum of C57Bl6 mice for 14 days. (elsevierpure.com)
  • 10. Neural Stem Cells of the Subventricular Zone Contribute to Neuroprotection of the Corpus Callosum after Cuprizone-Induced Demyelination. (nih.gov)
  • C57BL/6J mice were maintained on a cuprizone-containing or control diet and sacrificed at specific time points after initiation of treatment. (nih.gov)
  • tissue: brain age: adult genotype: B6N.129-Rpl22tm1.1Psam x B6.Synapsin1-Cre treatment: Cuprizone chow mice at 6 weeks on chow. (nih.gov)
  • 17. Anatomical Distribution of Cuprizone-Induced Lesions in C57BL6 Mice. (nih.gov)
  • We established an experimental system to measure the response latency of cortical neurons and examined changes in nerve conduction in cuprizone-induced demyelinating mice and in myelin basic protein-deficient shiverer mice. (elsevierpure.com)
  • The results of these electrophysiological assessments imply that different demyelinating mechanisms, differentially affecting axon conduction, are present in the cuprizone-treated and shiverer mice, and may provide new insights to understanding the pathophysiology of demyelination in animal models in the CNS. (elsevierpure.com)
  • A cuprizone (CPZ) -induced schizophrenic mice model was established. (jneuropsychiatry.org)
  • Astrocytes regulate myelin clearance through recruitment of microglia during cuprizone-induced demyelination. (semanticscholar.org)
  • Cortical demyelination is prominent in the murine cuprizone model and is strain-dependent. (semanticscholar.org)
  • In the present study, we used a murine model of cuprizone-induced demyelination to broaden the application of PBR as a marker of brain injury and to validate the relationship between PBR levels and glial cell types. (nih.gov)
  • 13. Lineage tracing reveals dynamic changes in oligodendrocyte precursor cells following cuprizone-induced demyelination. (nih.gov)
  • Our findings indicate that brain PBR levels increased as a function of dose and duration of cuprizone treatment and it was detectable prior to observable demyelination. (nih.gov)
  • 1991. A comparison of spongiosis induced in the brain by hexachlorophene, cuprizone and triethyl tin in the Sprague-Dawley rat. (nih.gov)
  • Interestingly, CDK5 exerts positive regulation in CPZ-induced autophagy, revealing that CDK5 overexpression enhances LC3â ¡ level and autophagosome formation in company with cuprizone treatment, while CDK5 knockdown works conversely. (jneuropsychiatry.org)
  • 6. The cuprizone model: regional heterogeneity of pathology. (nih.gov)
  • In vitro, cuprizone dose- and time-dependently induces excessive autophagy and autophagic flux, therefore depresses cell viability in oligodendrocytes. (jneuropsychiatry.org)
  • The data show that rhGas6 treatment resulted in more efficient repair following cuprizone-induced injury. (elsevierpure.com)
  • In this study, we tested the hypothesis that administration of recombinant human Gas6 (rhGas6) protein into the CNS improves recovery following cuprizone withdrawal. (elsevierpure.com)
  • In the present study, we used a murine model of cuprizone-induced demyelination to broaden the application of PBR as a marker of brain injury and to validate the relationship between PBR levels and glial cell types. (nih.gov)
  • Our findings indicate that brain PBR levels increased as a function of dose and duration of cuprizone treatment and it was detectable prior to observable demyelination. (nih.gov)
  • In this study, the contribution of myelin to both T(2)* and frequency contrasts is investigated using a mouse model of demyelination based on a cuprizone diet. (nih.gov)