Previous studies have found that AD-like pathological Aβ and hyperphosphorylated tau protein were degraded via the autophagic pathway [33], and the dysfunction of autophagy in different stages caused neurodegenerative diseases, including the dysfunction of AMPK-mTOR-mediated autophagy initiation [34], blocked APs degradation [35], and decreased autophagy–lysosome function [36]. The gene discussed is MTOR; the disease is Alzheimer disease.