ABSTRACT
Multiple sclerosis (MS) is an autoimmune disease characterized by attacks against components of the myelin sheath of the central nervous system (CNS) mediated by immuno-competent cells. In the early stages, distinct relapses are followed by remission and are often trailed by a chronic phase of disease with a progressive clinical course. Inflammation and demyelination are the most relevant physiopathological events of this disorder. Later in the disease course, axons, already damaged and devoid of the enveloping myelin sheath, degenerate through unknown mechanisms causing progressive worsening of the neurological condition.
