Recently, by using a mouse model of recurrent HSV-1 infection, we showed the long-term dangerous effects of repeated HSV-1 replications in the brain (e.g., Aβ accumulation and deposition in plaques, tau hyperphosphorylation and aggregation, neuroinflammation), providing a first demonstration of the cause–effect relationship between HSV-1 reactivations and accumulation of AD molecular hallmarks, including cognitive deficits [25] and impaired adult neurogenesis [26]. The gene discussed is MAPT; the disease is Cognitive impairment.