4.5 Article

Glia Disease and Repair - Remyelination

期刊

出版社

COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a020594

关键词

-

资金

  1. UK Multiple Sclerosis Society
  2. National Multiple Sclerosis Society
  3. National Institute of Neurological Disorders and Stroke (NINDS)
  4. National Institute of Mental Health (NIMH)
  5. New York State Stem Cell Research Program (NYSTEM)
  6. Adelson Medical Research Foundation
  7. Mathers Charitable Foundation
  8. Department of Defense
  9. Novo Nordisk Fonden [NNF13OC0004260] Funding Source: researchfish

向作者/读者索取更多资源

The inability of the mammalian central nervous system (CNS) to undergo spontaneous regeneration has long been regarded as a central tenet of neurobiology. However, although this is largely true of the neuronal elements of the adult mammalian CNS, save for discrete populations of granular neurons, the same is not true of its glial elements. In particular, the loss of oligodendrocytes, which results in demyelination, triggers a spontaneous and often highly efficient regenerative response, remyelination, in which new oligodendrocytes are generated andmyelin sheaths are restored to denuded axons. Yet, remyelination in humans is not without limitation, and a variety of demyelinating conditions are associated with sustained and disabling myelin loss. In this review, we will review the biology of remyelination, including the cells and signals involved; describewhen remyelination occurs and when and why it fails and the consequences of its failure; and discuss approaches for therapeutically enhancing remyelination in demyelinating diseases of both children and adults, both by stimulating endogenous oligodendrocyte progenitor cells and by transplanting these cells into demyelinated brain.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据