The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system.
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Oligodendrogenesis in the normal and pathological central nervous systemChondroitin sulfate proteoglycans in the nervous system: inhibitors to repairThe cyclooxygenase-2 pathway via the PGE₂ EP2 receptor contributes to oligodendrocytes apoptosis in cuprizone-induced demyelinationInhibition of p53 transcriptional activity: a potential target for future development of therapeutic strategies for primary demyelinationImaging of peripheral benzodiazepine receptor expression as biomarkers of detrimental versus beneficial glial responses in mouse models of Alzheimer's and other CNS pathologiesTranslocator protein 18 kDa (TSPO): molecular sensor of brain injury and repairBiomaterial Approaches to Enhancing Neurorestoration after Spinal Cord Injury: Strategies for Overcoming Inherent Biological ObstaclesThe unfolded protein response in multiple sclerosisDeletion of Jun proteins in adult oligodendrocytes does not perturb cell survival, or myelin maintenance in vivoDietary vitamin D3 supplements reduce demyelination in the cuprizone modelSpatial and temporal profiles of growth factor expression during CNS demyelination reveal the dynamics of repair primingDisruption of myelin leads to ectopic expression of K(V)1.1 channels with abnormal conductivity of optic nerve axons in a cuprizone-induced model of demyelinationIn vitro and in vivo induction and activation of nNOS by LPS in oligodendrocytesIntravenous transplantation of mouse embryonic stem cells attenuates demyelination in an ICR outbred mouse model of demyelinating diseasesGalanin transgenic mice with elevated circulating galanin levels alleviate demyelination in a cuprizone-induced MS mouse modelPolymorphisms in the receptor tyrosine kinase MERTK gene are associated with multiple sclerosis susceptibilityEffects of fumaric acids on cuprizone induced central nervous system de- and remyelination in the mouseAcrolein-mediated conduction loss is partially restored by K⁺ channel blockersAstrocyte-derived tissue Transglutaminase affects fibronectin deposition, but not aggregation, during cuprizone-induced demyelinationAge-dependent epigenetic control of differentiation inhibitors is critical for remyelination efficiencyDimensional assessment of behavioral changes in the cuprizone short-term exposure model for psychosisThe Cannabinoid CB1/CB2 Agonist WIN55212.2 Promotes Oligodendrocyte Differentiation In Vitro and Neuroprotection During the Cuprizone-Induced Central Nervous System Demyelination.Cuprizone short-term exposure: astrocytic IL-6 activation and behavioral changes relevant to psychosis.Behavioral and neurobiological changes in C57BL/6 mouse exposed to cuprizone: effects of antipsychotics.Downregulation of oligodendrocyte transcripts is associated with impaired prefrontal cortex function in rats.CXCR2-positive neutrophils are essential for cuprizone-induced demyelination: relevance to multiple sclerosisRostrocaudal analysis of corpus callosum demyelination and axon damage across disease stages refines diffusion tensor imaging correlations with pathological features.Myelin repair is accelerated by inactivating CXCR2 on nonhematopoietic cells.Inefficient clearance of myelin debris by microglia impairs remyelinating processesHistological correlation of diffusional kurtosis and white matter modeling metrics in cuprizone-induced corpus callosum demyelination.Understanding disease processes in multiple sclerosis through magnetic resonance imaging studies in animal models.In vivo quantification of demyelination and recovery using compartment-specific diffusion MRI metrics validated by electron microscopy.Role of tumour necrosis factor (TNF)-α and TNFRSF1A R92Q mutation in the pathogenesis of TNF receptor-associated periodic syndrome and multiple sclerosis.Therapeutic inhibition of soluble brain TNF promotes remyelination by increasing myelin phagocytosis by microgliaHistological validation of fast macromolecular proton fraction mapping as a quantitative myelin imaging method in the cuprizone demyelination modelIkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous systemGAS6 enhances repair following cuprizone-induced demyelination.Inhibition of Drp1 hyper-activation is protective in animal models of experimental multiple sclerosis.Heterogeneity in oligodendroglia: Is it relevant to mouse models and human disease?Mitochondrial immobilization mediated by syntaphilin facilitates survival of demyelinated axons.
P2860
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P2860
The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system.
description
2001 nî lūn-bûn
@nan
2001 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
The neurotoxicant, cuprizone, ...... in the central nervous system.
@ast
The neurotoxicant, cuprizone, ...... in the central nervous system.
@en
The neurotoxicant, cuprizone, ...... in the central nervous system.
@nl
type
label
The neurotoxicant, cuprizone, ...... in the central nervous system.
@ast
The neurotoxicant, cuprizone, ...... in the central nervous system.
@en
The neurotoxicant, cuprizone, ...... in the central nervous system.
@nl
prefLabel
The neurotoxicant, cuprizone, ...... in the central nervous system.
@ast
The neurotoxicant, cuprizone, ...... in the central nervous system.
@en
The neurotoxicant, cuprizone, ...... in the central nervous system.
@nl
P1433
P1476
The neurotoxicant, cuprizone, ...... in the central nervous system
@en
P2093
Matsushima GK
P304
P577
2001-01-01T00:00:00Z