Fonseca et al. (2009) observed complement activation in brains of a murine AD model, with the presence of complement proteins such as C1q, C3, and C4 in senile plaques and neurofibrillary tangles, which are hallmark features of the disease. Moreover, C1q, which binds to gC1qR, has been shown to bind to amyloid-beta (AB) peptide, which is a major component of the senile plaques in AD, and the binding of C1q to AB may trigger the complement cascade, resulting in inflammation and synaptic loss (Rogers et al., 1992; Hong et al., 2016). This evidence concerns the gene C3 and Alzheimer disease.