Demyelinating Diseases
Corpus Callosum
Myelin Sheath
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.
Oligodendroglia
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.
Monoamine Oxidase Inhibitors
Chelating Agents
Microglia
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.
Glial Fibrillary Acidic Protein
Gliosis
Astrocytes
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.
Brain-Derived Neurotrophic Factor
Receptor, trkB
Agenesis of Corpus Callosum
Birth defect that results in a partial or complete absence of the CORPUS CALLOSUM. It may be isolated or a part of a syndrome (e.g., AICARDI'S SYNDROME; ACROCALLOSAL SYNDROME; ANDERMANN SYNDROME; and HOLOPROSENCEPHALY). Clinical manifestations include neuromotor skill impairment and INTELLECTUAL DISABILITY of variable severity.
Nerve Fibers, Myelinated
A class of nerve fibers as defined by their structure, specifically the nerve sheath arrangement. The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH. They are fibers of relatively large and varied diameters. Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers (NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.
Antigens, CD47
Brain
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.
Neural Cell Adhesion Molecule L1
A member of the immunoglobulin superfamily of neuronal cell adhesion molecules that is required for proper nervous system development. Neural cell adhesion molecule L1 consists of six Ig domains, five fibronectin domains, a transmembrane region and an intracellular domain. Two splicing variants are known: a neuronal form that contains a four-amino acid RSLE sequence in the cytoplasmic domain, and a non-neuronal form that lacks the RSLE sequence. Mutations in the L1 gene result in L1 disease. Neural cell adhesion molecule L1 is predominantly expressed during development in neurons and Schwann cells; involved in cell adhesion, neuronal migration, axonal growth and pathfinding, and myelination.
Diffusion Tensor Imaging
Calcium Channels, T-Type
Zinc
A metallic element of atomic number 30 and atomic weight 65.38. It is a necessary trace element in the diet, forming an essential part of many enzymes, and playing an important role in protein synthesis and in cell division. Zinc deficiency is associated with ANEMIA, short stature, HYPOGONADISM, impaired WOUND HEALING, and geophagia. It is known by the symbol Zn.
Nociceptors
Peripheral AFFERENT NEURONS which are sensitive to injuries or pain, usually caused by extreme thermal exposures, mechanical forces, or other noxious stimuli. Their cell bodies reside in the DORSAL ROOT GANGLIA. Their peripheral terminals (NERVE ENDINGS) innervate target tissues and transduce noxious stimuli via axons to the CENTRAL NERVOUS SYSTEM.
Zinc Acetate
Calcium Channel Blockers
Ganglia, Spinal
Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.
Mibefradil
Prion Diseases
A group of genetic, infectious, or sporadic degenerative human and animal nervous system disorders associated with abnormal PRIONS. These diseases are characterized by conversion of the normal prion protein to an abnormal configuration via a post-translational process. In humans, these conditions generally feature DEMENTIA; ATAXIA; and a fatal outcome. Pathologic features include a spongiform encephalopathy without evidence of inflammation. The older literature occasionally refers to these as unconventional SLOW VIRUS DISEASES. (From Proc Natl Acad Sci USA 1998 Nov 10;95(23):13363-83)
PrPC Proteins
Prions
Small proteinaceous infectious particles which resist inactivation by procedures that modify NUCLEIC ACIDS and contain an abnormal isoform of a cellular protein which is a major and necessary component. The abnormal (scrapie) isoform is PrPSc (PRPSC PROTEINS) and the cellular isoform PrPC (PRPC PROTEINS). The primary amino acid sequence of the two isoforms is identical. Human diseases caused by prions include CREUTZFELDT-JAKOB SYNDROME; GERSTMANN-STRAUSSLER SYNDROME; and INSOMNIA, FATAL FAMILIAL.
Developmental Biology
PrPSc Proteins
Scrapie
Alzheimer Disease
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
Copper
Metals
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)
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HDAC1 nuclear export induced by pathological conditions is essential for the onset of axonal damage
Taurine Seen to Boost MS Therapies Efficacy in Remyelination Process
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Probing mouse brain microstructure using oscillating gradient diffusion MRI. | Kennedy Krieger Institute
Cell therapy promotes axon remyelination in a mouse model - Scienmag: Latest Science and Health News
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Demyelinating disease
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 ...
Glycolipid
"Cerebroside synthesis as a measure of the rate of remyelination following cuprizone-induced demyelination in brain". Journal of ...
Remyelination
... the resolution of status spongiosus and remyelination in cuprizone intoxication in mice". J. Neurocytol. 1 (4): 413-26. doi: ...
Hes3 signaling axis
... lacking mice also exhibit a different regulation of this protein after oligodendrocyte damage induced by the chemical cuprizone ...
GPR84
Elevated expression of GPR84 was also observed during the demyelination phase of the reversible Cuprizone-Induced Demyelinating ...
Cerebral edema
Toxic exposures to methionine sulfoxime, cuprizone, isoniazid, triethyl tin, hexachlorophene, and hydrogen cyanide have been ...
cuprizone | Journal of Neuroscience
The cuprizone animal model: new insights into an old story
... the cuprizone model reflects a toxic experimental model. Cuprizone-induced demyelination in animals is accepted for studying MS ... The cuprizone animal model: new insights into an old story Acta Neuropathol. 2009 Dec;118(6):723-36. doi: 10.1007/s00401-009- ... The present article reviews recent data concerning the cuprizone model and its relevance for MS. Particular focus is given to ... We also aim to distinguish acute and chronic demyelination under cuprizone including processes such as spontaneous ...
Astrocyte-Derived BDNF Supports Myelin Protein Synthesis after Cuprizone-Induced Demyelination | Journal of Neuroscience
After cuprizone, the HA+ non-GFAP+ cells are greatly reduced. When cuprizone-treated mice are injected with ACPD, there is an ... Cuprizone treatment. Demyelination was initiated by feeding 8-week-old wild-type male mice or HA male mice 0.2% cuprizone ( ... To evaluate the effects of ACPD in the cuprizone model, wild-type mice treated with cuprizone received a single stereotaxic ... Wild-type mice were fed control or cuprizone-laden food for 4 weeks. NF-L+ axons fail to colocalize with (a) mGluR1, or (b) ...
WikiGenes - Cuprizone - N,N'-bis(cyclohexylideneamino)ethanediamide
Cuprizone-induced demyelination is a mouse model of multiple sclerosis (MS) as cuprizone-fed mice exhibit neuroinflammation and ... High impact information on Cuprizone. *The membrane potentials of giant mitochondria from cuprizone-fed mice were found to be ... Biological context of Cuprizone. *When 8 week old C57BL/6 mice are fed 0.2% cuprizone in the diet, mature olidgodendroglia are ... Dietary supplementation with cuprizone or with cuprizone + copper sulfate resulted in considerably depressed (20-50%) rates of ...
Neural Stem Cells of the Subventricular Zone Contribute to Neuroprotection of the Corpus Callosum after Cuprizone-Induced...
Using transgenic mice to fate map and to selectively kill SVZ-derived eNPCs in the cuprizone demyelination model, we observed ... First, we fate mapped SVZ-eNPCs in cuprizone-induced demyelination and found that SVZ endogenous neural stem/precursor cells ... When we ablated SVZ-derived eNPCs during cuprizone-induced demyelination in female mice, the animals displayed reduced numbers ... Neural Stem Cells of the Subventricular Zone Contribute to Neuroprotection of the Corpus Callosum after Cuprizone-Induced ...
Neurotoxicity of Cuprizone in Female and Male Rats: Electrophysiological Observations | Springer for Research & Development
... the effects of cuprizone on the functions of the peripheral nervous system, as well as differential effects it may exert on ... Cuprizone induces massive demyelination in the CNS; however, ... Cuprizone led to a reduction in the NCV, CMAP amplitude and ... Cuprizone induces massive demyelination in the CNS; however, the effects of cuprizone on the functions of the peripheral ... S. Love, "Cuprizone neurotoxicity in the rat: Morphologic observations," J. Neurol. Sci., 84, Nos. 2/3, 223-237 (1988).CrossRef ...
Neuroprotective effect of linagliptin against cuprizone-induced demyelination and behavioural dysfunction in mice: A pivotal...
C57Bl/6 mice were fed chow containing 0.7% cuprizone for 1 week, followed by 3 weeks of a 0.2% cuprizone diet. Linagliptin (10 ... Linagliptin attenuated cuprizone-induced oxidative stress by decreasing brain thiobarbituric acid reactive substances along ... Home » Topics » Spinal Cord Disorders » Research » Neuroprotective effect of linagliptin against cuprizone-induced ... This study investigated the possible neuroprotective effect of linagliptin against cuprizone-induced demyelination in mice and ...
Effect of Multiple Intraperitoneal Injections of Human Bone Marrow Mesenchymal Stem Cells on Cuprizone Model of Multiple...
We aimed to investigate the effect of multiple i.p. BM-MSCs injections in the cuprizone model of multiple sclerosis in mice. ... Methods: Adult male C57BL/6 mice (n = 40) were fed a regular diet or a diet containing cuprizone (0.2% w/w) for 6 six weeks. ... We aimed to investigate the effect of multiple i.p. BM-MSCs injections in the cuprizone model of multiple sclerosis in mice. ... Cuprizone could decrease myelin-binding protein mRNAs expression in corpus callosum, which was significantly recovered after BM ...
Chronic white matter atrophy after acute cuprizone exposure may be.... ECTRIMS Online Library. Caprariello A. Oct 12 2018;...
The Cuprizone Mouse Model | Multiple Sclerosis Discovery Forum
In the acute cuprizone paradigm, male C57BL/6 mice at 6 to 9 weeks of age are fed a diet of chow mixed with 0.2% cuprizone over ... Cuprizone is heat-sensitive, so it is recommended that it be stored at between 2-8°C to retain effectiveness. Cuprizone chow ... Cuprizone (bis-cyclohexanone oxaldihydrazone) can be purchased from Sigma-Aldrich (cat# C9012). To add cuprizone to standard ... oral administration of cuprizone produces a global insult. Different rodent strains react in idiosyncratic ways to cuprizone, ...
Frontiers | Deletion of CD38 Suppresses Glial Activation and Neuroinflammation in a Mouse Model of Demyelination | Cellular...
To analyze its role in the demyelinating situation, we employed cuprizone (CPZ)-induced demyelination model in mice, which is ... To analyze its role in the demyelinating situation, we employed cuprizone (CPZ)-induced demyelination model in mice, which is ... Cuprizone Administration. To induce demyelination in 10-week-old ICR male mice, they were administered a diet containing 0.4% ... Cuprizone (CPZ)-induced experimental demyelination is a suitable rodent model to study the mechanisms leading to demyelination ...
"Leucine Supplementation in Cuprizone-Induced Oligodendrocyte Toxicity" by Michael Ley
... can increase cell vitality after being treated with cuprizone. Additional studies examined the solubility of cuprizone and ... In this proposal, we further examine the chemical and toxicological properties of cuprizone. Immunofluorescence imaging and ... Taken altogether, this experiment reveals that cuprizone affects lysosomal and mitochondrial function, and provides insight ... Cuprizone is a copper chelator that induces demyelination in the central nervous system when fed to mice. This compound is ...
Frontiers | Pre-clinical and Clinical Implications of "Inside-Out" vs. "Outside-In" Paradigms in Multiple Sclerosis...
Cuprizone Autoimmune Encephalitis (CAE) Model. In addition to diphtheria-toxin, cuprizone is a demyelinating neurotoxin that ... Long-term of cuprizone feeding in mice lead to oligodendrocyte death, demyelination and gliosis (Matsushima and Morell, 2001; ... 2015). Thymic atrophy and apoptosis of CD4+CD8+ thymocytes in the cuprizone model of multiple sclerosis. PLoS One 10:e0129217. ... Sen, M. K., Mahns, D. A., Coorssen, J. R., and Shortland, P. J. (2019b). Behavioural phenotypes in the cuprizone model of ...
Promotion of remyelination by adipose mesenchymal stem cell transplantation in a cuprizone model of multiple sclerosis | Cell...
Animals were fed with 0.2% w/w cuprizone added to ground breeder chow ad libitum for six weeks. At day 0 after cuprizone ... Index: IMEMR (Eastern Mediterranean) Main subject: Adipose Tissue / Cuprizone / Mesenchymal Stem Cell Transplantation / Mice ... Promotion of remyelination by adipose mesenchymal stem cell transplantation in a cuprizone model of multiple sclerosis ... Promotion of remyelination by adipose mesenchymal stem cell transplantation in a cuprizone ...
Ameliorative effects of Moringa on cuprizone-induced memory decline in rat model of multiple sclerosis | Anatomy & Cell...
Four groups of rats were treated with normal saline, cuprizone, M. oleifera and a combination of M. oleifera and cuprizone, for ... Cuprizone is a neurotoxin with copper-chelating ability used in animal model of multiple sclerosis in which oxidative stress ... Animals , Brain , Catalase , Cuprizone , Hippocampus , Memory , Memory, Short-Term , Models, Animal , Moringa oleifera , ... Cuprizone significantly induced oxidative and nitrosative stress coupled with memory decline and cortico-hippocampal neuronal ...
Intracerebral transplantation of interleukin 13-producing mesenchymal stem cells limits microgliosis, oligodendrocyte loss and...
... as compared to cuprizone-treated mice with control MSC grafts and/or cuprizone-treated mice without MSC injection. In the first ... Next, CNS inflammation and demyelination was induced by means of a cuprizone-supplemented diet. The influence of IL13-MSC ... limits cuprizone-induced microgliosis, oligodendrocyte death and demyelination. Furthermore, we here demonstrate that injection ... and to interfere with oligodendrocyte death and demyelinating events in the cuprizone mouse model. ...
Cannabidiol Displays Proteomic Similarities to Antipsychotics in Cuprizone-Exposed Human Oligodendrocytic Cell Line MO3.13
These general pathways are associated with cuprizone-induced cytotoxicity in MO3.13 cells, indicating a possible proteomic ... In conclusion, although modeling oligodendrocytic cytotoxicity with cuprizone does not represent the entirety of the ... Cannabidiol Displays Proteomic Similarities to Antipsychotics in Cuprizone-Exposed Human Oligodendrocytic Cell Line MO3.13. ... and clozapine modulated cell proliferation and apoptosis when administered after cuprizone-induced toxicity. ...
Microglial SIRPα regulates the emergence of CD11c+ microglia and demyelination damage in white matter | eLife
... without cuprizone)" and at "3 and 5 weeks cuprizone feeding" in the new Figure 8. Unfortunately, we could not expand the data ... Alleviation of cuprizone-induced demyelination in SIRPα cKO mice.. (A) Control (SIRPα-flox:- (Ctrl)) or SIRPα cKO (SIRPα-flox: ... Cuprizone model of demyelination. Request a detailed protocol Control (SIRPα-flox:-) or SIRPα cKO (SIRPα-flox:Cx3cr1CreERT2) ... Alleviation of cuprizone-induced demyelination in the brain white matter of microglia-specific SIRPα-deficient mice. Although ...
Reducing Agents Sensitize C-Type Nociceptors by Relieving High-Affinity Zinc Inhibition of T-Type Calcium Channels | Journal of...
... cuprizone, 111 ± 3%; n = 6-8, *p , 0.01. E, Time course and raw traces comparing the effects of cuprizone, tricine, and l-cys ... Bovine serum albumin (BSA), DTT, l-cys, l-histidine (L-his), tricine, and Zn2+ were dissolved in H2O; cuprizone, 5,5′dithio-bis ... whereas the relatively Cu2+-selective chelator cuprizone effected a smaller, but significant, current increase (Fig. 4D,E). ...
Expression of the low-affinity neurotrophin receptor, p75(NTR), is upregulated by oligodendroglial progenitors adjacent to the...
JCI -
Peripherally derived FGF21 promotes remyelination in the central nervous system
Demyelination by cuprizone diet. Mice were placed on a diet of 0.2% (wt/wt) cuprizone mixed into chow pellets. Mice were ... MH helped with tamoxifen injection and cuprizone feeding. HF, MY, and HM provided autopsied samples. M Konishi and NI ... Peripheral macrophage recruitment in cuprizone-induced CNS demyelination despite an intact blood-brain barrier. J Neuroimmunol ... Kondo A, Nakano T, Suzuki K. Blood-brain barrier permeability to horseradish peroxidase in twitcher and cuprizone-intoxicated ...
Hematopoietic cell activation in the subventricular zone after Theiler's virus infection | Journal of Neuroinflammation | Full...
Cuprizone induced demyelination. Chow containing 0.2% cuprizone (Harlan Teklad) was fed to C57Bl mice (N = 7) ad libitum for 3 ... Cuprizone demyelination does not cause CD45 activation in the SVZ. A, B) CD45 expression is minimal in control corpus callosum ... Cuprizone induced demyelination does not induce CD45 activation in the SVZ. We next asked whether the massive CD45 cell ... Cuprizone, a copper chelating agent induces demyelination in a variety of CNS regions including immediately above the SVZ, in ...
The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system. | Multiple...
Changes of thymic endocrine function, brain macrophages and T-lymphocytes in mice of different ages after administration of...
The 129/Sv mice received cuprizone with food daily for 3 weeks. From day 8 of cuprizone diet, the rhLIF was injected daily (50 ... In cuprizone-treated mice of both age groups (especially in young), the number of brain T-cells increased. RhLIF injections ... The effect of both cuprizone and rhLIF on thymic endocrine function and the number of brain macrophages and T-lymphocytes in ... Hormone level decreased after 3-week cuprizone treatment only in young mice. After 7 days, the number of brain macrophages in ...
Demyelination and Remyelination | The New York Academy of Sciences
PET imaging of demyelination and remyelination in the cuprizone mouse model for multiple sclerosis: a comparison between [11C] ... Transplantation into adult shiverer mice resulted in phenotypic rescue; it also ameliorated demyelination in a cuprizone mouse ... 2. Focus on benztropine; PLP-induced EAE model; T cell independent cuprizone model*. 11:03 ... with demyelination chemically induced using cuprizone) suggested that benzatropine works by enhancing myelination. However, ...
Kjell-Morten Myhr | Universitetet i Bergen
Torkildsen, Øivind Fredvik; Brunborg, Linn Anne Bjelland; Myhr, Kjell-Morten; Bø, Lars. 2008. The cuprizone model for ... Wergeland, Stig; Torkildsen, Øivind; Myhr, Kjell-Morten; Mørk, Sverre; Bø, Lars. 2012. The cuprizone model: regional ... A salmon based diet protects mice from behavioural changes in the cuprizone model for demyelination. Clinical Nutrition. 83-87 ... Fish diet prevents impaired mobility in the murine cuprizone model for multiple sclerosis. Multiple Sclerosis. S90-S91. ...
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Microglial SIRPα regulates the emergence of CD11c+ microglia and demyelination damage in white matter. - PubMed - NCBI
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Christakoudi, S., Tsilidis, K. K., Muller, D. C., Freisling, H., Weiderpass, E., Overvad, K., Söderberg, S., Häggström, C., Pischon, T., Dahm, C. C., Zhang, J., Tjønneland, A., Halkjær, J., MacDonald, C., Boutron-Ruault, M-C., Mancini, F. R., Kühn, T., Kaaks, R., Schulze, M. B., Trichopoulou, A. & 27 others, Karakatsani, A., Peppa, E., Masala, G., Pala, V., Panico, S., Tumino, R., Sacerdote, C., Quirós, J. R., Agudo, A., Sánchez, M-J., Cirera, L., Barricarte-Gurrea, A., Amiano, P., Memarian, E., Sonestedt, E., Bueno-de-Mesquita, B., May, A. M., Khaw, K-T., Wareham, N. J., Tong, T. Y. N., Huybrechts, I., Noh, H., Aglago, E. K., Ellingjord-Dale, M., Ward, H. A., Aune, D. & Riboli, E., 3 Sep 2020, In: Scientific Reports. 10, 1, 15 p., 14541.. Research output: Contribution to journal › Journal article › Research › peer-review ...
Multiple SclerosisMyelinResearchers stopped feeding the mice tOxidative stressDemyelination in the corpus callosumCorpusC57BLToxicityModelInducesExperimentalOligodendrocytesProliferationDysfunction in miceChowAlterationsReproducesOrallyLesionsAblationChronicMO3.13DeficitsTransplantationWeeksRatsRegenerationAnimalsAffectsExposureDietAdministrationTreatmentEffectsBrainZincLimitsConclusionProtein
Multiple Sclerosis4
- BM-MSCs injections in the cuprizone model of multiple sclerosis in mice. (ac.ir)
- BM-MSCs in the cuprizone model of multiple sclerosis in mice. (ac.ir)
- Cuprizone is a neurotoxin with copper-chelating ability used in animal model of multiple sclerosis in which oxidative stress has been documented as one of the cascade in the pathogenesis. (bvsalud.org)
- Her team was recently awarded a pilot grant from the National Multiple Sclerosis Society to compare postmortem brain tissue from MS patients with seizures to those without to understand the cellular basis of seizures in MS. Their findings will also be used to check how well the cuprizone mouse model reproduces the changes seen in humans. (eurekalert.org)
Myelin10
- Cuprizone-induced demyelination in animals is accepted for studying MS-related lesions and is characterized by degeneration of oligodendrocytes rather than by a direct attack on the myelin sheet. (nih.gov)
- Psychological stress effects on myelin degradation in the cuprizone-induced model of demyelination. (bioportfolio.com)
- Cuprizone could decrease myelin-binding protein mRNAs expression in corpus callosum, which was significantly recovered after BM-MSCs injections. (ac.ir)
- In conclusion, although modeling oligodendrocytic cytotoxicity with cuprizone does not represent the entirety of the pathophysiology of oligodendrocyte impairments, these results provide insight into the mechanisms associated with the effects of cannabidiol and antipsychotics against cuprizone toxicity, offering new directions of study for myelin-related processes and deficits. (medicalcannabisbelgique.com)
- In the lab, Tiwari-Woodruff and her team induced demyelination in mice by feeding them a diet that contained cuprizone, a copper-binding substance that causes damage to oligodendrocytes -the brain cells that produce myelin. (eurekalert.org)
- In one UCR study, the six-person team fed mice cuprizone, a copper-binding substance that damages brain cells that produce myelin, for nine weeks and found the mice later had seizures. (pe.com)
- In the cuprizone model of oligodendrocyte degeneration and demyelination, Trem2 -/- microglia failed to amplify transcripts indicative of activation, phagocytosis, and lipid catabolism in response to myelin damage. (jci.org)
- As a result, Trem2 -/- mice exhibited impaired myelin debris clearance, axonal dystrophy, oligodendrocyte reduction, and persistent demyelination after prolonged cuprizone treatment. (jci.org)
- The present study aims to assess the effects of the cannabinoid agonist WIN-55,212-2 in cuprizone fed animals on myelin repair capacity. (thisisms.com)
- Animals exposed to cuprizone were simultaneously treated withWIN-55,212-2, behaviorally tested and finally the corpus callosum was exhaustively studied by Western blotting, qRT-PCR and a myelin staining procedure. (thisisms.com)
Researchers stopped feeding the mice t1
- In another study, after nine or twelve weeks, the researchers stopped feeding the mice the cuprizone diet. (eurekalert.org)
Oxidative stress1
- Linagliptin attenuated cuprizone-induced oxidative stress by decreasing brain thiobarbituric acid reactive substances along with restoring reduced glutathione levels. (bioportfolio.com)
Demyelination in the corpus callosum1
- Histologically, cuprizone induced demyelination in the corpus callosum. (ac.ir)
Corpus9
- Neural Stem Cells of the Subventricular Zone Contribute to Neuroprotection of the Corpus Callosum after Cuprizone-Induced Demyelination. (nih.gov)
- First, we fate mapped SVZ-eNPCs in cuprizone-induced demyelination and found that SVZ endogenous neural stem/precursor cells are recruited during the remyelination phase to the corpus callosum (CC) and are capable of forming new oligodendrocytes. (nih.gov)
- By the third week of cuprizone feeding, consistent demyelination can be observed in the corpus callosum, the largest white matter tract in the mouse brain. (msdiscovery.org)
- In this study، the effects of Vitamin D3 on total protein concentration (TPC) and MBP expression in the corpus callosum extracts of Cuprizone induced demyelinated mouse has been investigated. (magiran.com)
- It is concluded that vitamin D3 increases MBP expression in the corpus callosum of cuprizone-induced demyelination mice. (magiran.com)
- 3) Functional assessment with DBSI: Currently, Abby applies DBSI/dfMRI to study optic nerve and corpus callosum of EAE, cuprizone, traumatic brain injury (TBI), and Huntington's disease mice to understand interplay of function deficits and pathology in CNS. (wustl.edu)
- D-F) Representative confocal images of GFP + cells (green) and immunoreactive Iba1 + cells (red) in the hippocampus and corpus callosum of chimeric mice either untreated (D) or after 5 wk of treatment with a cuprizone diet in GFP (E) and CCR2 −/− (F) chimeric mice. (rupress.org)
- Demyelination and remyelination in anatomically distinct regions of the corpus callosum following cuprizone intoxication. (tamu.edu)
- Deleting Lrp1 from adult OPCs also increases the number of newborn mature OLs added to the corpus callosum in response to cuprizone-induced demyelination. (edu.au)
C57BL4
- C57Bl/6 mice were fed chow containing 0.7% cuprizone for 1 week, followed by 3 weeks of a 0.2% cuprizone diet. (bioportfolio.com)
- Adult male C57BL/6 mice (n = 40) were fed a regular diet or a diet containing cuprizone (0.2% w/w) for 6 six weeks. (ac.ir)
- Different rodent strains react in idiosyncratic ways to cuprizone, which is best characterized in the C57BL/6 strain. (msdiscovery.org)
- In the acute cuprizone paradigm, male C57BL/6 mice at 6 to 9 weeks of age are fed a diet of chow mixed with 0.2% cuprizone over the course of 6 weeks. (msdiscovery.org)
Toxicity2
- For this purpose, we employed nano-chromatography coupled with mass spectrometry to investigate the proteomic response to these drugs both in healthy oligodendrocytic cells and in a cuprizone-based toxicity model, using the human oligodendrocyte precursor cell line MO3.13. (medicalcannabisbelgique.com)
- All drugs tested affected metabolic and gene expression pathways and cannabidiol, benztropine, and clozapine modulated cell proliferation and apoptosis when administered after cuprizone-induced toxicity. (medicalcannabisbelgique.com)
Model17
- While experimental allergic encephalomyelitis is one of the most frequently used models to investigate MS pathology and therapeutic interventions, the cuprizone model reflects a toxic experimental model. (nih.gov)
- The present article reviews recent data concerning the cuprizone model and its relevance for MS. Particular focus is given to the concordance and difference between human MS patterns (types I-IV lesions) and cuprizone-induced histopathology, including a detailed description of the sensitive brain regions extending the observations to different white and grey matter structures. (nih.gov)
- Finally, we point at strain and gender differences in this animal model and highlight the contribution of some growth factors and cytokines during and after cuprizone intoxication, including LIF, IGF-1, and PDGFalpha. (nih.gov)
- Using transgenic mice to fate map and to selectively kill SVZ-derived eNPCs in the cuprizone demyelination model, we observed migration of SVZ-eNPCs after injury and their contribution to oligodendrogenesis and axonal survival. (nih.gov)
- Arecoline attenuates memory impairment and demyelination in a cuprizone-induced mouse model of schizophrenia. (bioportfolio.com)
- A common model of acute demyelination oral administration of copper-depleting cuprizone (CPZ) holds promise for defining mechanisms of progressive degeneration. (ectrims-congress.eu)
- The cuprizone mouse model captures several aspects of MS pathology, bypassing the autoimmune component in other preclinical models. (msdiscovery.org)
- Gender is another rate-limiting factor to consider when using the cuprizone model. (msdiscovery.org)
- Wendy Macklin's laboratory has recently developed a technique to better separate the demyelination and remyelination phases of the cuprizone model. (msdiscovery.org)
- To analyze its role in the demyelinating situation, we employed cuprizone (CPZ)-induced demyelination model in mice, which is characterized by oligodendrocyte-specific apoptosis, followed by the strong glial activation, demyelination, and repopulation of OLs. (frontiersin.org)
- Controlled and localised production of IL13 by means of intracerebral MSC grafting has the potential to modulate cell graft- and pathology-associated microglial/macrophage responses, and to interfere with oligodendrocyte death and demyelinating events in the cuprizone mouse model. (biomedcentral.com)
- Charles River offers cuprizone- and lysolecithin-induced rodent models of demyelination to test novel therapies for MS. The cuprizone model uses a validated study design where demyelination is induced followed by a recovery period of remyelination. (criver.com)
- What are some of the parameters that change in the cuprizone model of MS? (criver.com)
- BM-derived cells are recruited in a CCR2-dependent manner into demyelinating sites of the CNS in the cuprizone model. (rupress.org)
- This model of experimental MS in mice is widely used because cuprizone administration causes an artificial demyelination reaction through oligodendrocyte apoptosis, while its withdrawal leads to spontaneous remyelination. (medworm.com)
- Toll-Like Receptor 2-Mediated Glial Cell Activation in a Mouse Model of Cuprizone-Induced Demyelination. (uni-muenchen.de)
- Early regional cuprizone-induced demyelination in a rat model revealed with MRI. (mbfbioscience.com)
Induces2
- Prolonged cuprizone exposure induces chronic demyelination and impairs the capacity of the brain to repair. (msdiscovery.org)
- Cuprizone is a copper chelator that induces demyelination in the central nervous system when fed to mice. (uakron.edu)
Experimental4
- The combined use of chronic and relapsing remitting experimental autoimmune encephalomyelitis (C-EAE, R-EAE) ("outside-in") as well as progressive diphtheria toxin A chain ( DTA) and cuprizone autoimmune encephalitis (CAE) ("inside-out") mouse models allow for the investigation and specific targeting of all three of these MS-associated disease parameters. (frontiersin.org)
- The EAE (experimental autoimmune encephalomyelitis) series of MS models are widely used to test therapies targeting the inflammation component of MS, while MS models where demyelination is induced by cuprizone, lysolecithin, or ethidium bromide are increasingly being used to test therapeutic candidates. (criver.com)
- The present study evaluated the protective effect of melatonin on demyelination and remyelination processes in male and female mice with experimental MS induced by cuprizone. (medworm.com)
- Trem2 -/- mice also differ from wild-type mice in their responses to experimental demyelination induced by oral administration of the copper chelator cuprizone (CPZ). (alzforum.org)
Oligodendrocytes1
- When we ablated SVZ-derived eNPCs during cuprizone-induced demyelination in female mice, the animals displayed reduced numbers of oligodendrocytes within the lesioned CC. Although this reduction in oligodendrocytes did not impact the ensuing remyelination, eNPC-ablated mice experienced increased axonal loss. (nih.gov)
Proliferation1
- When administered orally in mice, cuprizone, a copper chelator, causes rapid demyelination and gliosis, or rapid proliferation of glia subtypes. (msdiscovery.org)
Dysfunction in mice1
- Neuroprotective effect of linagliptin against cuprizone-induced demyelination and behavioural dysfunction in mice: A pivotal role of AMPK/SIRT1 and JAK2/STAT3/NF-κB signalling pathway modulation. (bioportfolio.com)
Chow1
- Animals were fed with 0.2% w/w cuprizone added to ground breeder chow ad libitum for six weeks. (bvsalud.org)
Alterations4
- Immunofluorescence imaging and microarray data on MO3.13 cells treated with cuprizone revealed the possibility of alterations in lysosomal function, as well as mitochondrial disruption via mTOR and Electron Transport Chain (ETC) related pathways. (uakron.edu)
- This study aimed at evaluating the ameliorative capability of M. oleifera in cuprizone-induced behavioral and histopathological alterations in the prefrontal cortex and hippocampus of Wistar rats. (bvsalud.org)
- The influence of IL13-MSC grafting on neuropathological alterations was monitored by non-invasive T 2 -weighted magnetic resonance imaging (MRI) and quantitative histological analyses, as compared to cuprizone-treated mice with control MSC grafts and/or cuprizone-treated mice without MSC injection. (biomedcentral.com)
- Lack of cuprizone-induced demyelination in the murine spinal cord despite oligodendroglial alterations substantiates the concept of site-specific susceptibilities of the central nervous system. (tiho-hannover.de)
Reproduces1
- The tissue study, which was recently funded by the National MS Society, will investigate how much cuprizone-fed mice research reproduces changes in humans. (pe.com)
Orally1
- Cuprizone was orally administered at a dose of 400 mg/kg/day by oral gavage for 5 weeks. (medworm.com)
Lesions2
- Similarities between pattern III lesions and cuprizone-induced demyelination and dissimilarities, such as inflamed blood vessels or the presence of CD3+ T cells, are outlined. (nih.gov)
- In adult mice, Sema6A expression is upregulated in demyelinating lesions in cuprizone-treated mice. (wingsforlife.com)
Ablation1
- In addition, cuprizone-induced demyelination was alleviated by the microglia-specific ablation of SIRPα. (elifesciences.org)
Chronic2
- We also aim to distinguish acute and chronic demyelination under cuprizone including processes such as spontaneous remyelination during acute demyelination. (nih.gov)
- Chronic white matter atrophy after acute cuprizone exposure may be. (ectrims-congress.eu)
MO3.131
- These general pathways are associated with cuprizone-induced cytotoxicity in MO3.13 cells, indicating a possible proteomic approach when acting against the toxic effects of cuprizone. (medicalcannabisbelgique.com)
Deficits2
- however, administration of M. oleifera significantly reversed the neuropathological deficits induced by cuprizone. (bvsalud.org)
- dfMRI differentiated functional deficits in CC of cuprizone mice. (wustl.edu)
Transplantation1
- 6 wk after transplantation, 0.2% Cuprizone was added to the diet for up to 6 wk. (rupress.org)
Weeks8
- BM-MSCs (2 × 10 6 in 1 milliliter medium) were administered intraperitoneally for two consecutive weeks at the end of the forth weeks of cuprizone administration. (ac.ir)
- With cuprizone alone, her laboratory documents 30% to 40% myelination at 6 weeks, with remyelination complete by 3 to 5 weeks off the toxicant. (msdiscovery.org)
- With cuprizone and rapamycin together, the group detects 0% myelination at 6 weeks and complete remyelination 7 weeks later. (msdiscovery.org)
- Four groups of rats were treated with normal saline, cuprizone, M. oleifera and a combination of M. oleifera and cuprizone, for five weeks. (bvsalud.org)
- The mice were treated by Cuprizone for five weeks in order to induce demyelination. (magiran.com)
- After nine weeks of feeding them cuprizone, the majority of mice started having seizures. (eurekalert.org)
- In a second study, researchers stopped feeding the mice cuprizone after nine or 12 weeks. (pe.com)
- Histological analysis revealed clear demyelination after being fed cuprizone for three weeks. (thisisms.com)
Rats2
- Thus, we aimed to examine changes in the electromyographic characteristics of female and male Sprague-Dawley rats with cuprizone-induced demyelination. (springer.com)
- Notably, electrophysiological observations reveal that cuprizone affects both female and male rats, but males are more sensitive. (springer.com)
Regeneration1
- Loss of Nampt reduces neural stem/progenitor cell‐derived oligodendrocyte regeneration after cuprizone‐induced demyelination. (embopress.org)
Animals1
- During the second course of Cuprizone, the animals showed greater resistance to the toxin and demyelination occurred slowly and was complete only after prolonged periods. (docme.ru)
Affects1
- Taken altogether, this experiment reveals that cuprizone affects lysosomal and mitochondrial function, and provides insight into leucine supplementation at an attempt to rescue cells from neurotoxicity. (uakron.edu)
Exposure1
- The animal's gender, age, and exposure time to cuprizone are important determinants of the reproducibility and sequence of de- and remyelination events. (msdiscovery.org)
Diet2
- Next, CNS inflammation and demyelination was induced by means of a cuprizone-supplemented diet. (biomedcentral.com)
- Another group was sacrificed 2 wk after removing cuprizone from the diet to allow remyelination. (rupress.org)
Administration2
- Unlike other toxicant-induced models, which are introduced in the brain by stereotaxic microinjections and result in focal demyelination, oral administration of cuprizone produces a global insult. (msdiscovery.org)
- J Am Vet Med Assoc 169:228-229, 1976 Evidence for a "Dying-Back" Gliopathy in Demyelinating Disease samuel K. ~ ~ dMB, ~ ~ ic h~ , , and Edward S. Johnson, MD# Recurrent demyelination was produced in mice by Cuprizone administration. (docme.ru)
Treatment2
- Linagliptin treatment improved behavioural and motor abnormalities induced by cuprizone, as demonstrated by open field, rotarod and grip strength tests. (bioportfolio.com)
- Cuprizone treatment is the most frequently used among the toxicant-induced MS models, which include lysolecithin and ethidium bromide, and is used to study mechanisms of oligodendrocyte turnover, astrogliosis, and microgliosis ( Blakemore and Franklin, 2008 ). (msdiscovery.org)
Effects1
- however, the effects of cuprizone on the functions of the peripheral nervous system, as well as differential effects it may exert on males and females, have not yet been studied. (springer.com)
Brain1
- 1991. A comparison of spongiosis induced in the brain by hexachlorophene, cuprizone and triethyl tin in the Sprague-Dawley rat. (nih.gov)
Zinc1
- Additional studies examined the solubility of cuprizone and interaction with zinc. (uakron.edu)
Limits1
- In the second part of this study, we demonstrate that grafting of IL13-MSC, in addition to the recruitment of M2 polarised macrophages, limits cuprizone-induced microgliosis, oligodendrocyte death and demyelination. (biomedcentral.com)
Conclusion1
- In conclusion, linagliptin exerted a neuroprotective effect in mice with cuprizone-induced demyelination possibly by modulating AMPK/SIRT1 and JAK2/STAT3/NF-κB signalling pathways. (bioportfolio.com)
Protein1
- The Anti-Aging Protein Klotho Enhances Remyelination Following Cuprizone-Induced Demyelination. (bu.edu)