title: Remyelinating the demyelinated CNS.
abstract: The CNS has an inherent capacity to generate remyelinating cells following episodes of myelin loss. However, persistent demyelination is the major pathology of multiple sclerosis and the leucodystrophies, and is also a feature of spinal cord trauma. There are potentially two approaches for achieving remyelination in situations where it fails; enhancement of the inherent remyelinating capacity of the CNS, or transplantation of an exogenous source of myelin forming cells. In experimental animals it is possible to remyelinate demyelinated CNS axons by transplanting cultures containing central or peripheral myelinogenic cells. Glial cell transplantation may thus provide a therapeutic strategy for remyelinating areas of chronic demyelination as well as for stimulating axon regeneration. This presentation will review four issues that have to be addressed before glial transplantation can be undertaken in humans: is the procedure safe, what cells would be used, where would the cells come from and can we predict how much remyelination will be achieved? It concludes that the most promising approach will be to use multipotent neural precursor cells that have been committed to oligodendrocyte lineage differentiation prior to implantation. However, even with such preparations, which have considerable myelinating potential, the extent of remyelination that would be achieved can not yet be predicted with any degree of certainty.
authors.affiliation: Department of Clinical Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, UK.
authors.forename: W F
authors.initials: WF
authors.lastname: Blakemore
authors.forename: P M
authors.initials: PM
authors.lastname: Smith
authors.forename: R J
authors.initials: RJ
authors.lastname: Franklin
mesh_terms: D000818:Animals; D016380:Brain Tissue Transplantation; D003711:Demyelinating Diseases / Q000473:pathology; D006801:Humans; D009103:Multiple Sclerosis / Q000473:pathology / Q000601:surgery*; D009186:Myelin Sheath / Q000473:pathology; D009474:Neurons / Q000637:transplantation*; D013106:Sphingolipidoses / Q000473:pathology / Q000601:surgery