Complements are deposited in senile plaques, neurofibrillary tangles, and blood vessels. Microglia is activated around these structures and induce chronic inflammation through a cross talk between microglia and astroglia. Complements activated by amyloidβ (Aβ) bind to complement receptor (CR3) and help phagocytosis of the aggregated Aβ via opsonization of the aggregated Aβ. Inflammation in capillary cerebral amyloid angiopathy (CAA) may suppress Aβclearance and trigger a vicious cycle aggravating CAA.