A key early eventin AD pathogenesis is the misfolding and aggregationof Aβ, followed by tau aggregation, neuronal loss, and ultimatelymore severe pathological events and clinical manifestations.7,8 Blocking Aβ aggregation is thus a promising therapeutic target.Recent findings have revealed several anti-infectives can interferewith aggregation of amyloidogenic proteins like Aβ, tau, andα-synuclein, positioning them as potential repurposing agentsagainst amyloid aggregation in neurodegenerative diseases.9 The gene discussed is MAPT; the disease is neurodegenerative disease.