In terms of early complement proteins, C1q, C3b, C4b, and properdin have all been localized to key pathological hallmarks of AD, such as amyloid plaques and neurofibrillary tangles (hyperphosphorylated τ) in human AD and animal models, supporting the activation of both classical and alternative pathways in vivo (reviewed in Fonseca et al., 2011; Veerhuis, 2011). The gene discussed is C3; the disease is Alzheimer disease.