Abstract
Neuromyelitis optica (NMO) is a rare demyelinating disorder haracterized by recurrent optic neuritis and longitudinal extensive ransverse myelitis (LETM). The pathogenesis of NMO is still under xtensive study with recent findings supporting the pathological ole for humoral immunity, with the production of anti-aquaporinautoantibodies of the IgG class combined with the activation of he complement cascade [1,2]. These data indicate a distinctive athology of NMO compared to MS and recognition of NMO as a eparate disease entity. The pathological role of anti-aquaporin-4 utoantibodies (anti-AQP4 Ab) depends on induction of astroyte dysfunction resulting in oligodendrocyte loss [3,4]. 68–91% of atients with NMO have circulating IgG1 Abs against aquaporin(AQP4), termed NMO-IgG [5] a water channel protein expressed ainly in the central nervous system (CNS) in the plasma memrane of astrocytes [6]. NMO is a rare disorder and only since it as been distinguished from multiple sclerosis are data regarding he course of disease and effects of treatment starting to appear. In
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