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Remyelination after spinal cord injury: Is it a target for repair?

期刊

PROGRESS IN NEUROBIOLOGY
卷 117, 期 -, 页码 54-72

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2014.02.006

关键词

Spinal cord injury; Oligodendrocyte; Remyelination; Myelin; Oligodendrocyte precursor cell; Axon degeneration

资金

  1. Canadian Instates of Health Research (CIHR)
  2. MS Society of Canada
  3. Heart and Stroke Foundation of Canada
  4. Alberta Prion Research Institute-Alberta ingenuity
  5. Alberta Heritage Foundation Medical Research
  6. Alberta Cancer Foundation
  7. Donna Joan Oxford MS Society of Canada
  8. Alberta Innovates - Health Solutions

向作者/读者索取更多资源

After spinal cord injury (SCI) there is prolonged and dispersed oligodendrocyte cell death that is responsible for widespread demyelination. To regenerate this lost myelin, many investigators have transplanted myelin-producing cells as a treatment for contusive SCI. There are several documented examples of cellular transplantation improving function after injury, with the degree of myelin regeneration correlating with functional recovery. On the basis of these findings, remyelination is hypothesized to be a beneficial strategy to promote recovery after injury. As cellular transplantation is now entering clinical trials for treatment of SCI, it is important to dissect carefully whether accelerating remyelination after SCI is a valid clinical target. In this review we will discuss the consequences of demyelination and the potential benefits of remyelination as it relates to injury. Prolonged demyelination is hypothesized to enhance axonal vulnerability to degeneration, and is thereby thought to contribute to the axonal degeneration that underlies the permanent functional losses associated with SCI. Currently, strategies to promote remyelination after SCI are largely limited to cellular transplantation. This review discusses those strategies as well as new, and largely untested, modes of therapy that aim to coax endogenous cells residing adjacent to the injury site to differentiate in order to replace lost myelin. (C) 2014 Elsevier Ltd. All rights reserved.

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