Autophagy is a natural degradation process for removing unnecessary or dysfunctional cellular components via a lysosome-dependent mechanism. Dysfunctional autophagy is known to contribute to neurodegeneration 518 while improvement of autophagy has been believed to be useful for treating a variety of disorders, including metabolic disorders, neurodegenerative and infectious diseases, and cancers. An unharmed autophagy performance in neurons exhibits a neuroprotective effect since autophagy expedites the elimination of pathogenic kinds of proteins such as α-synuclein involved in Parkinson's disease 519 or tau-protein in Alzheimer's disease. Therapy involving autophagy enhancers such as rapamycin and lithium have been reported to engender favorable effects in animal models of Parkinson's disease, such as reduced α-synuclein aggregation, oxidative stress, mitochondrial dysfunction, and neurodegeneration. Delaying aging and stimulating longevity achieved through food deprivation and caloric restriction are facilitated through upregulation of autophagy because reducing autophagy diminishes the anti-aging outcomes of caloric restriction. Furthermore, studies have indicated that enhancing autophagy could reinstate the regenerative capacity of aging stem cells. Thus, autophagy enhancing interventions would likely facilitate successful aging and increased longevity.