AQP4 and neuromyelitis optica: The selective loss of peri-plaque synapses observed in models and man suggests an additional mechanism whereby complement activation on plaques initiates bystander injury of adjacent synapses through seeding of MAC precursors (Fig. 5c); a precedent has been reported in neuromyelitis optica, where aquaporin-4 autoantibodies trigger complement activation on astrocytes, releasing MAC precursors that seed damaging MAC assembly on nearby neurons [68].