In more recent studies in other AD models, C1q was found to be increased and deposited at synapses before overt plaque deposition, whereas deletion of C1q or C3 or the complement receptor CR3 (also expressed on microglia), reduced the number of phagocytic microglia as well as the extent of early synapse loss, resulting in improved cognitive function (Hong et al., 2016; Figure 2B). Here, C3 is linked to Alzheimer disease.