Multiple sclerosis (MS) is an autoimmune demyelinating disease which affects the central nervous system (CNS). 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. As the 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. Histopathological evidence suggests that activated microglia are a central feature in both inflammatory non-demyelinating and active demyelinating lesions within MS brains obtained at autopsy, which decorate these plaque areas and persist for the duration of the disease. It has been shown that microglia/macrophage activation can be rapidly stimulated or reversed depending on the extracellular stimuli applied. Upon activation, microglia release excessive pro-inflammatory mediators, which can induce the generation of cytokines, nitric oxide, reactive oxygen species and glutamate, contributing to tissue damage; the cells may also scavenge damaged myelin/axonal debris Alrehaili A, et al., Microglial Mechanisms Governing Axonal Degeneration in Multiple Sclerosis: A Pathological Perspective.
It is essential to focus on this major area of multiple sclerosis research because the identification of pathology of the disease favors the researchers to find a cure for this dreadful menace. Thus journal of multiple sclerosis considers this as a main area of focus in journal discussion forums.
Last date updated on June, 2014