作者: Natalie A. Wheeler , Babette Fuss
DOI: 10.1016/J.EXPNEUROL.2016.03.019
关键词:
摘要: There is an increasing number of neurologic disorders found to be associated with loss and/or dysfunction the CNS myelin sheath, ranging from classic demyelinating disease, multiple sclerosis, through injury, neuropsychiatric diseases. The disabling burden these diseases has sparked a growing interest in gaining better understanding molecular mechanisms regulating differentiation myelinating cells CNS, oligodendrocytes (OLGs), and process (re)myelination. In this context, importance extracellular milieu becoming increasingly recognized. Under pathological conditions, changes inhibitory as well permissive/promotional cues are thought lead overall environment that obstructive for regeneration sheath. Given general view remyelination is, even though limited human, natural response demyelination, targeting pathologically 'dysregulated' their downstream pathways regarded promising approach toward enhancement by endogenous (or if necessary transplanted) OLG progenitor cells. review, we will introduce have been implicated modulation These can soluble, part matrix (ECM) or mediators cell-cell interactions. Their roles regard potential therapeutic intervention discussed.