Mitochondrial dysfunction and autophagy in neurodegeneration

Abstract Mitochondria play a multifactorial role in regulating cellular and biological processes for the maintenance in neural circuit and integrity. Principal reasons behind many neurodegenerative disorders (NDD) are mitochondrial dysfunction and increased production of reactive oxygen species (ROS). ROS is responsible for brain ailments such as Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Huntington’s Disease (HD), and Amyotrophic Lateral Sclerosis (ALS). Additionally, calcium influx disrupts oxidative phosphorylation (OXPHOS) and increases oxidative stress, that eventually alters mitochondrial function and damages the autophagic as well as endosomal-lysosomal pathway. Thus, targeting the mitochondrial pathway through redox signaling has been identified as a therapeutic approach in the prevention of impaired autophagy-induced NDDs. Herein, we discussed, how oxidative stress, modulating the mitochondrial functions and autophagic pathways, is involved in the pathogenesis of NDDs. Lastly, we described the pharmacological approaches to prevent mitochondrial function and impaired autophagic clearance.