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Multiple sclerosis (MS) is a demyelinating and inflammatory disease of the central nervous system (CNS). The destruction of the oligodendrocyte-derived myelin lamellae leads to loss of nerve insulation and results in impairment of fast saltatory conduction. Axons and neurons are also damaged and lost in the disease process (1), and cell repopulation is hampered by the inability of mature neurons to undergo cell division. An attractive approach for reestablishing electrochemical circuits in MS would be to restore the function or number of myelin-generating oligodendrocytes in early lesions, to act as bridges that guide and promote axonal regeneration. [ABSTRACT FROM AUTHOR]