Myelination of the Central Nervous System

Multiple sclerosis (MS) results from a combination of genetically determined susceptibility, environmental factors, viral or bacterial agents, soluble cytokines released during the inflammatory and autoimmune responses, and probably other, as yet undetermined etiologic agents. The disease can cause variable degrees of tissue destruction in the central nervous system (CNS), ranging from marginal demyelination to complete oligodendrocyte loss, severe glial scarring [1], and axonal transection. In some instances oligodendrocytes are morphologically preserved in demyelination plaques and remain capable of differentiating and remyelinating, as shown in humans and various model systems [1, 3]. In other cases, however, oligodendrocytes vanish and progenitors have to migrate into the plaque and proliferate. Adult oligodendrocyte progenitors are different from their post-natal counterparts, but seem to retain the ability to migrate and proliferate under the influence of specific growth factors [4]. However, the proliferating pool is limited, as is its ability to migrate [5, 6].