A recently proposed mechanism holds that complement-mediated synaptic pruning that is dormant in the adult brain becomes active in AD and mediates synaptic loss, with accumulation of oligomeric Aβ and hyperphosphorylated Tau leading to astrocyte overexpression of complement C1q and C3, which prime synapses for microglial phagocytosis [30,54,56,57]. The gene discussed is C3; the disease is Alzheimer disease.