Abstract

Neuromyelitis optica (NMO) and NMO spectrum disorders (NMOSD) have garnered attention due to their high pathogenicity, high risk of relapse, and poor prognosis as an inflammatory central nervous system (CNS) syndrome. There is a consensus that the anti-aquaporin-4 antibody (AQP4-IgG) is the main pathogen detectable in majority of NMOSD patients, including traditional NMO and AQP4-IgG-positive optic neuritis. In serum-negative NMOSD patients, myelin oligodendrocyte glycoprotein (MOG) antibodies are considered pathogenic factors. At present, patients with NMO optic neuritis (NMO-ON) hardly benefit from common therapies. A limitation of studies on NMO-ON is the inadequacy of animal models. This review article focuses on the characteristics of visual impairments in NMOSD and the application of experimental rodent models which are required for elucidating the pathology and potential treatments for NMO visual impairment.

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