The hyperactivity of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mTOR cascade, mediated by the phosphorylation of INSR via insulin binding to the neuronal surface, leads to the inhibition of autophagy processes and subsequent accumulation of damaged mitochondria and misfolded proteins seen in AD [19]. This evidence concerns the gene AKT1 and Alzheimer disease.