Year: 2017
Type: article
Abstract: BACKGROUND: Multiple sclerosis (MS) is a severe neurological disorder, characterized by demyelination of the central nervous system (CNS), and with a prevalence of greater than 2 million people worldwide. In terms of research in MS pathology, the cuprizone toxicity model is widely used. Here we investigated the contribution of genetic differences in response to cuprizone-induced demyelination in two genetically different mouse strains: CD1 and C57BL/6. RESULTS: We demonstrate that exposure to a diet containing 0.2% cuprizone resulted in less severe demyelination in the midline of the corpus callosum over the fornix in CD1 mice than C57BL/6 mice. With continuous cuprizone feeding, demyelination in CD1 mice was not prominent until after 7 weeks, in contrast to C57BL/6 mice, which showed prominent demyelination after 4 weeks of exposure. Concomitantly, immunohistochemical analysis demonstrated more oligodendrocytes, as well as fewer oligodendrocyte progenitor cells, microglia and astrocytes in cuprizone treated CD1 mice. We also analyzed 4-weeks-cuprizone treated corpus callosum tissue samples and found that cuprizone treated CD1 mice showed a smaller reduction of myelin-associated glycoprotein (MAG) and a smaller increase of Iba1 and NG2. CONCLUSIONS: These observations suggest that CD1 mice are less vulnerable to cuprizone-induced demyelination than C57BL/6 mice and thus genetic background factors appear to influence the susceptibility to cuprizone-induced demyelination.
Source: Cell & Bioscience
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,890
Funders: National Multiple Sclerosis Society, National Institutes of Health, National Institute of Mental Health, National Eye Institute, National Institute of Neurological Disorders and Stroke, National Institute of Environmental Health Sciences, Eunice Kennedy Shriver National Institute of Child Health and Human Development
Awards: Regulation of Lens Fiber Cell Organization, The Role of Neurotrophins in Oligodendrocyte Function, Maternal Immune Effects on Neurobehavioral Development, The Role of Neurotrophins in Oligodendrocyte Function, Growth and Develoment of the Nervous System: Molecular Mechanisms, G723235710, Role of Orphanin/FQ in the Behavioral and Neuroinflammatory Response to Stress, G9000020500, Rutgers Center for Environmental Exposure and Disease (CEED)
OpenAlex ID: W2766251897