Interestingly, the mechanism by which synapse loss is induced by Aβ oligomers, proximal synaptotoxins in AD[31], involves complement components C1q and C3 via microglia-mediated phagocytosis in which these molecules tag synapses and bind receptors on microglia, eliminating them in young mice injected with Aβ oligomers in the absence of Aβ plaques[26].Complement activation is crucial in the interaction between astrocytes and microglia, serving a protective function during the early stages of Alzheimer’s disease. The gene discussed is C3; the disease is Alzheimer disease.