Triggers for conversion may arise from diverse sources and include age-related changes to the levels of amyloidogenic proteins (Aβ in AD), predisposition of proteins to adopt pathologic conformations (e.g., α-SN in sporadic PD), genetic alterations that augment the amyloidogenic propensity of proteins (e.g., polyglutamine expansion of the HTT gene in Huntington’s disease) and abnormal post-translational modifications (e.g., Tau hyperphosphorylation in AD)1. The gene discussed is MAPT; the disease is Alzheimer disease.