For instance, the genetic deletion of the complement factors C1q and complement component 3 (C3) or the microglial complement receptor CR3 decreases the early synapse loss and the number of activated microglia, which, by provoking the induction of phagocytic microglia, is suggestive of complement activation as an early mediator for plaque-associated synapse loss in AD brains [38,39,40]. This evidence concerns the gene C3 and Alzheimer disease.