Do central nervous system axons remyelinate?

In multiple sclerosis (MS), one of the most frequent demyelinating diseases in man, remyelination of demyelinating lesions exists but is often incompl ete. Also reported in experimental models of demyelination, this phenomenom confirms the regenerating potential of the demyelinated central nervous sy stem (CNS) and, in particular, the existence of an endogenous mechanism of oligodendrocyte renewal. Failure in efficient remyelination could result fr om exhaustion of the pool of remyelinating cells, loss of axons and absence of a permissive environment for remyelination. Identifying the nature and the origin of the cells capable of generating new oligodendrocytes for remy elination could contribute to strategies to activate these cells, and there by enhance their potential for myelin repair. Within the adult CNS, several cell types are capable of generating new oligodendrocytes following myelin damage: post-mitotic oligodendrocytes frequently found at the lesion site, oligodendrocyte progenitors whose existence has been confirmed both in vit ro and in vivo, and multipotent cells localized in the germinative areas of the brain and the spinal cord. Although restricted to particular sites of the CNS, these multipotent cells, which maintain the capacity to self-renew and to migrate throughout adulthood, could constitute a powerful source of remyelinating cells. The study of the mechanisms of proliferation, migrati on and differentiation of these cells in response to demyelination should a llow the definition of new strategies to promote endogenous remyelination a nd develop therapeutic approaches for demyelinating diseases such as MS. Th is goal is an appealing alternative to the transplantation of myelin-formin g cells and should efficiently complement strategies aimed at reducing neur onal loss and inflammation. (C) 2000 Editions scientifiques et medica[es El sevier SAS.