also found that selenomethionine (Se‐Met) therapy can improve cognitive deficits in triple transgenic AD (3xTg‐AD) mice through two patterns: (1) the inhibition Tau hyperphosphorylation by regulating Akt (protein kinase B), glycogen synthase kinase 3β and PP2A activities; (2) autophagy initiation can activate the AMPK‐mTOR signaling pathway, and promote Tau clearance in AD neurons [115, 116]. This evidence concerns the gene AKT1 and Alzheimer disease.