Abstract

Multiple sclerosis (MS) is presumably an immune mediated disease of the human central nervous system with two salient pathophysiologic components: inflammatory demyelination and neurodegeneration. Both arms of MS pathophysiology cause loss of myelin sheath and myelin-producing cells, oligodendrocytes. Existing therapies for MS are based heavily on suppression of the peripheral immune system, with no significant impact on neurodegeneration and repair of lost myelin. The remyelination process is expected to restore normal neuronal activity and repair some of the existing injury to the CNS. However, the remyelination process is often overwhelmed by the demyelinating process, and in that condition, the outcome will be neuronal and axonal loss, along with accumulating disability for the MS patient.

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