Abstract
In multiple sclerosis (MS) some areas of demyelination remyelinate while the majority do not. On the basis that it is possible to myelinate myelin-deficient areas by glial cell transplantation in experimental models (Lachapelle et al.1984; Blakemore and Crang, 1988; Blakemore et al.1995; Duncan, 1996), it may be possible to remyelinate areas of persistent demyelination in MS by introducing cells with remyelinating potential. However, if one is to predict the outcome of such a procedure it is necessary to understand the basis for success or failure of endogenous remyelination in MS, since it may be a basic property of this demyelinating disease that some areas of demyelination can be remyelinated while others cannot. If the latter situation pertains in areas of chronic demyelination, introducing cells with remyelinating potential will either have no effect or will only be of limited benefit. In order to understand why remyelination should fail in some lesions and not others, and thereby design a transplant strategy that is likely to be successful, it is necessary to resolve a number of inter-related issues that include; what cell gives rise to remyelinating oligodendrocytes, over what distance can such cells be recruited into an area of demyelination, can cells migrate freely within the adult CNS and within areas of demyelination? This article will address the first of these issues.
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Blakemore, W.F., Crang, A.J., Keirstead, H.S., Franklin, R.J.M. (1997). Recent Insights into the Cellular Biology of Remyelination. In: Juurlink, B.H.J., Devon, R.M., Doucette, J.R., Nazarali, A.J., Schreyer, D.J., Verge, V.M.K. (eds) Cell Biology and Pathology of Myelin. Altschul Symposia Series, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5949-8_23
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DOI: https://doi.org/10.1007/978-1-4615-5949-8_23
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