Inhibitory milieu at the multiple sclerosis lesion site and the challenges for remyelination |
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Authors: | Dylan A. Galloway Elizabeth Gowing Solmaz Setayeshgar Rashmi Kothary |
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Affiliation: | 1. Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada;2. Neurosciences Department, Faculty of Medicine, Centre de recherche du CHUM, Université de Montreal, Montreal, Quebec, Canada;3. Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada;4. Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada |
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Abstract: | Regeneration of myelin, following injury, can occur within the central nervous system to reinstate proper axonal conductance and provide trophic support. Failure to do so renders the axons vulnerable, leading to eventual degeneration, and neuronal loss. Thus, it is essential to understand the mechanisms by which remyelination or failure to remyelinate occur, particularly in the context of demyelinating and neurodegenerative disorders. In multiple sclerosis, oligodendrocyte progenitor cells (OPCs) migrate to lesion sites to repair myelin. However, during disease progression, the ability of OPCs to participate in remyelination diminishes coincident with worsening of the symptoms. Remyelination is affected by a broad range of cues from intrinsic programming of OPCs and extrinsic local factors to the immune system and other systemic elements including diet and exercise. Here we review the literature on these diverse inhibitory factors and the challenges they pose to remyelination. Results spanning several disciplines from fundamental preclinical studies to knowledge gained in the clinic will be discussed. |
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Keywords: | exercise immune system microbiome microRNA myelin repair nutrition oligodendrocyte |
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