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Dietary influence on central nervous system myelin production, injury, and regeneration

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ELSEVIER
DOI: 10.1016/j.bbadis.2020.165779

关键词

Diet; Myelin; Multiple sclerosis; Oligodendrocyte; Astrocyte; Inflammation; Regeneration; Lifestyle modification; Repair; Remyelination

资金

  1. Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (CMSAN)
  2. Craig H. Neilsen Foundation
  3. Eugene and Marcia Applebaum Foundation
  4. Mayo Clinic Center for Biomedical Discovery

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Oligodendrocytes not only produce myelin to facilitate nerve impulse conduction, but are also essential metabolic partners of the axon. Oligodendrocyte loss and myelin destruction, as occurs in multiple sclerosis (MS), leaves axons vulnerable to degeneration and permanent neurological deficits ensue. Many studies now propose that lifestyle factors such as diet may impact demyelinating conditions, including MS. Most prior reviews have focused on the regulatory role of diet in the inflammatory events that drive MS pathogenesis, however the potential for dietary factors to modulate oligodendrocyte biology, myelin injury and myelin regeneration remain poorly understood. Here we review the current evidence from clinical and animal model studies regarding the impact of diet or dietary factors on myelin integrity and other pathogenic features of MS. Some limited evidence exists that certain foods may decrease risk or influence the progression of MS, such as increased intake of fish or polyunsaturated fatty acids, caloric restriction and fasting-mimicking diets. In addition, evidence suggests adolescent obesity or insufficient vitamin D levels increase the risk for developing MS. However, no clear or consistent evidence exists that dietary components exacerbate disease progression. Cumulatively, current evidence highlights the need for more extensive clinical trials to validate dietary effects on MS and to identify diets or supplements that may be beneficial as food-based strategies in the management of MS alone or in combination with conventional disease modifying therapies.

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