Multiple sclerosis (MS) and neuromyelitis optica (NMO) are inflammatory demyelinating diseases of the central nervous system (CNS). The pathological hallmark of MS is sharply demarcated demyelinating plaques with the relative preservation of axons, suggesting autoimmune responses target CNS myelin. In contrast, NMO shows selective and severe attacks of both axons and myelin of the optic nerves and spinal cord, resulting in necrotic cavitation. Neuropathological studies have demonstrated extensive loss of aquaporin-4 (AQP4) and glial fibrillary acidic protein (GFAP) in NMO lesions, especially in perivascular areas of acute inflammatory lesions where immunoglobulins and activated complements are deposited. We recently demonstrated the extensive loss of connexins(Cxs) in active lesions of Baló's disease, MS and NMO. Early disruption of Cx gap junction among glial cells may be a common denominator in heterogeneous human demyelinating conditions. This review aims to discuss the molecular pathology of MS and NMO that have attracted the most attention in the recent years.
|Number of pages||9|
|Journal||Nihon rinsho. Japanese journal of clinical medicine|
|Publication status||Published - Nov 1 2014|
All Science Journal Classification (ASJC) codes