In addition, loss-of-function mutations in several genes with autophagy-related function such as Becn1/VPS30/ATG6 (90), Atg7 (91), and Atg5 (92) can result in dysfunctional autophagy and increased accumulation of disordered and aggregated proteins such as Aβ and Tau in AD, indicating that autophagy failure has become an important therapeutic target for AD and regulating autophagy by exogenous means may become a new strategy for AD treatment. This evidence concerns the gene ATG5 and Alzheimer disease.