AI Article Synopsis

  • MS is the most common neurological autoimmune disorder in young adults, marked by demyelinating lesions in the central nervous system (CNS).
  • Three strategies to promote remyelination are growth factor application, myelin-forming cell transplantation, and intravenous immunoglobulin (IVIg) therapy, though challenges exist with growth factors and cell transplants.
  • Recent research suggests that IVIg therapy shows promise for promoting remyelination in humans, leading to ongoing exploration of myelin sheath development and oligodendrocyte differentiation in relation to MS treatment.

Article Abstract

Multiple sclerosis (MS), the most common neurological autoimmune disorder diagnosed in young adults, is characterised by the repeated occurrence of demyelinating lesions within the central nervous system (CNS). Promotion of remyelination in the brain and spinal cord constitutes a potential strategy for therapeutic intervention in MS and other demyelinating diseases. Three different principles are known to promote remyelination in the CNS of different animal models: Application of growth factors, transplantation of myelin-forming cells and intravenous immunoglobulin (IVIg) therapy. However, the systemic application of growth factors could be limited by effects on unaffected tissue. For successful transplantation we still have the problem of homologous cells not tolerated by a immunological different organism. Currently the required combination of growth factors needed to cultivate human homologous cells is not known, so that cells suitable for transplantation are still not available. Nevertheless, there is increasing evidence for beneficial effects of IVIg therapy on the promotion of remyelination in humans. In this review we summarise recent findings on the regulation of myelin sheath development and oligodendrocyte differentiation, and discuss the presented strategies in the context of possible clinical application for the therapy of MS.

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http://dx.doi.org/10.1007/s001150050352DOI Listing

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