Abstract
Neuromyelitis optica spectrum disorder (NMOSD) is caused by antibodies that target the aquaporin-4 (AQP4) water channel expressed on astrocytes. Specific antibody binding to AQP4 produces complement-dependent cytotoxicity, resulting in inflammation and demyelination. New biologic treatments demonstrate high efficacy and good safety for patients with AQP4-immunoglobulin G-positive NMOSD. They were eculizumab, an anti-complement C5 antibody, satralizumab, an anti-interleukin-6 receptor antibody, and inebilizumab and rituximab, which targets CD19 and CD20, respectively, causing depletion of B-cells. In this review, the pathophysiology of NMOSD, the methodology and results of the recent studies examining monoclonal antibody therapies, and the optimal therapeutic strategy for NMOSD were covered.
Publisher
Korean Society of Neuroimmunology