Compelling evidence has shown that in AD, infections with pathogens such as herpes simplex virus 1, oral porphyromonas gingivalis, and abnormal gut microbiota can induce anti-pathogen accumulation of beta-amyloid, cause beta-amyloid to misfold and aggregate which triggers tau aggregation (90), and thus these pathogen infections evoke the formation of “prions” that conforms normal beta-amyloid and tau proteins to pathological prion-like beta-amyloid and tau proteins (3, 88, 89). The gene discussed is MAPT; the disease is infection.