The genes encoding the complement system proteins complement receptor 1 (CR1) and clusterin are top hits in AD genome-wide association studies (GWAS),14,15 while fluid (plasma and CSF) and tissue complement biomarker studies in AD provide evidence of complement dysregulation early in the disease course.10,16,17 Complement deficiency in animal models of AD has been shown to prevent or ameliorate disease.18-21 Collectively, the data implicate complement as a driver of neuroinflammation and resultant neurodegeneration in AD. This evidence concerns the gene CLU and Alzheimer disease.