Multiple sclerosis (MS) is defined as a probable autoimmune disease that severely affects the central nervous system (CNS), resulting in several pathologies that may be a result of different disease-causing mechanisms. Classically characterised by extensive demyelination, which is associated with perivascular leukocyte infiltration in the active lesions and inflammation in the brain and spinal cord, gliosis and axonal damage or loss. Considered to be the main cause of non-traumatic primary neurological disability in young adults, affecting approximately 1:1000 individuals in Europe and North America with specific epidemiological ââ¬Åhot-spotsââ¬Â. The pathogenesis of the disease has been attributed to specific adaptive immune mechanisms preliminary defined through the vast array of experimentally induced encephalitis animal models. However, there is a growing body of evidence which report that innate immune players contribute to the disease course with extensive activation of endogenous microglia being a primary feature. Disease progresses, the substantial CNS degeneration can be correlated histopathologically with amoeboid microglia and numerous studies report this activity as central to the disease course of MS
Last date updated on September, 2024