Abstract
Autophagy involves degradation of dysfunctional cellular components through the actions of lysosomes. Apoptosis is the process of programmed cell death involving a series of characteristic cell changes. Autophagy and apoptosis, as self-destructive processes, play an important role in the pathogenesis of neurological diseases; and a crosstalk between "self-eating" (autophagy) and "self-killing" (apoptosis) plays an important role in pathological cellular adaptation. Expert knowledge of autophagy and apoptosis has increased in recent years, particularly in regards to cellular and molecular mechanisms. The crosstalk between autophagy and apoptosis was partially uncovered and several key molecules, including Bcl-2 family members, Beclin 1, and p53 were identified. However, the precise mechanisms of such a crosstalk remain to be elucidated. This current review article aims to summarize key mediators of the autophagy-apoptosis crosstalk in pathological conditions, and to highlight recent advances in the field, as well as to discuss further investigations and therapeutic potentials of manipulating those mechanisms in central nervous system diseases.