Intersection between Redox Homeostasis and Autophagy: Valuable Insights into Neurodegeneration

Autophagy, a main degradation pathway for maintaining cellular homeostasis, and redox homeostasis have recently been considered to play protective roles in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Increased levels of reactive oxygen species (ROS) in neurons can induce mitochondrial damage and protein aggregation, thereby resulting in neurodegeneration. Oxidative stress is one of the major activation signals for the induction of autophagy. Upon activation, autophagy can remove ROS, damaged mitochondria, and aggregated proteins from the cells. Thus, autophagy can be an effective strategy to maintain redox homeostasis in the brain. However, the interaction between redox homeostasis and autophagy is not clearly elucidated. In this review, we discuss recent studies on the relationship between redox homeostasis and autophagy associated with neurodegenerative diseases and propose that autophagy induction through pharmacological intervention or genetic activation might be a promising strategy to treat these disorders.

Automated summary

Autophagy and redox homeostasis play protective roles in neurodegenerative diseases, with oxidative stress being a major signal for Autophagy induction. Autophagy can remove ROS and damaged organelles to maintain redox balance in the brain, but the interaction between redox homeostasis and Autophagy is not fully understood. Pharmacological or genetic induction of Autophagy may be a promising strategy for treating neurodegenerative disorders.