In the context of Alzheimer's disease (AD) pathology, overproduction of AD promote the release of C3 from astrocytes, which simultaneously communicate with microglial C3aR and neuronal C3aR to dynamically regulate microglial phagocytosis and impair dendritic morphology as well as synaptic function, subsequently deteriorate cognitive function. The gene discussed is C3AR1; the disease is early-onset autosomal dominant Alzheimer disease.