The role of domain alterations in F1Fo-ATPase dysfunction associated to neurodegenerative diseases

Abstract

Mitochondrial dysfunction can lead to degeneration in the central nervous system. F1Fo-ATPase catalyzes most of the intracellular ATP synthesis which plays an essential role in cellular energy supply. The dimerized assembly of F1Fo-ATPase underlies the rotational catalytic function and regulates the mechanisms of oxidative phosphorylation. F1Fo-ATPase dysfunction is involved in a variety of neurological diseases, including epilepsy, Alzheimer's disease, and Parkinson’s disease. Dysregulated expression, activity, and localization of F1Fo-ATPase subunits and the interactions with pathogenic proteins result in decreased F1Fo-ATPase activity and ATP production, and aggravated oxidative stress.