Synergy between the pathophysiology of AD and long COVID is supported by evidence for shared genetic vulnerability to COVID-19 and AD, as well as common mechanistic pathways including microglia-mediated neuroinflammation, tau hyperphosphorylation, and amyloid-β accumulation (Golzari-Sorkheh et al., 2023), underscoring the need for further research into the effects of long COVID on the precipitation of AD and related dementias. The gene discussed is MAPT; the disease is COVID-19.