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Neuromyelitis optica spectrum disorder (NMOSD) is an antibody-mediated autoimmune disease of the central nervous system (CNS), typically characterized by optic neuritis and myelitis.Aquaporin-4 antibodies initiate astrocyte injury, although the factors triggering their production are unclear.Subsequent interactions among astrocytes, microglia, complement and peripheral immune cells drive neuroinflammation, demyelination and axonal damage.Microglia amplify tissue injury through the release of inflammatory mediators and cytotoxic factors, while contributing to debris clearance and tissue repair.The present review examines the roles of microglia in NMOSD, with a focus on complement, cytokine and interferon signaling, lipid metabolism and metabolic reprogramming.It further discusses therapeutic strategies for modulating microglial activity and the challenges of translating experimental findings into clinical practice.Elucidating the context-dependent balance between inflammatory and reparative microglial states may facilitate the development of strategies that limit immune-mediated injury while promoting CNS recovery.
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Zhang et al. (2026) studied this question.
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