Abstract

Publisher Summary In the central nervous system (CNS), the processes of oligodendrocytes (OLs), one of the major classes of glial cells, enwrap axons to form the myelin sheaths. These sheaths act as insulators and increase the efficiency and velocity of the propagation of nerve impulses along axons. Damage to, and loss of myelin impairs conduction, and as a result, the functions mediated by the demyelinated fibres, even when the axons remain intact. In man, this process of demyelination is seen in a number of diseases of which the commonest is multiple sclerosis (MS). Although there is substantial evidence that replacement of OLs, reensheathment of axons— that is, remyelination, and restoration of conduction occurs in many experimental models of demyelinating disease, myelin repair in MS is often scant or absent, especially during chronic stages of the disease. Little is known about the underlying cause of the myelin destruction in MS and about why repair of MS lesions is not sustained. This chapter discusses the advances that have increased the understanding of both the cellular mechanisms and factors that control the generation of OLs in the normal and demyelinated adult rodent CNS and the reasons for the failure of myelin repair in MS, with particular emphasis on OL precursor cells. Finally, potential strategies to enhance remyelination in MS are discussed briefly.

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