ABSTRACT
Multiple sclerosis (MS), an inflammatory demyelinating disease of the human central nervous system (CNS), is the most common cause of acquired nontraumatic neurologic disability in young adults. The pathologic hallmarks of the disease include damage to oligodendrocytes and CNS myelin, with subsequent demyelination, axonal loss and glial scarring. Active areas of disease display a prominent inflammatory response with tissue infiltration by mononuclear cells, primarily T-cells and macrophages. Although the exact causes of tissue damage in MS are largely unknown, the accumulation of demyelinated lesions probably accounts, at least in part, for the development of the neurologic deficits that are observed in patients with MS. Therapeutic strategies designed to promote remyelination may therefore hold promise for the treatment of this disease.
