In neuromyelitis optica spectrum disorder (NMOSD), pathogenesis involves pathogenic anti-aquaporin-4 (AQP4) antibodies mediating astrocyte damage through activation of the complement cascade, antibody-dependent cellular cytotoxicity (ADCC), and inflammatory cytokine release, ultimately leading to blood–brain barrier (BBB) disruption, demyelination, and secondary neuronal injury. Here, AQP4 is linked to neuromyelitis optica.