Previously, we showed that a well-known antibiotic, rifampicin, inhibits the aggregation of amyloidogenic proteins, including Aβ, tau, and α-synuclein, in vitro and improves cognition in mouse models of Alzheimer’s disease (AD), tau-associated FTD, and dementia with Lewy bodies (DLB) [32,33]. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.