Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer’s disease

Abstract

F1FO ATP synthase is a critical enzyme for the maintenance of mitochondrial function. Here the authors demonstrate that loss of the F1FO-ATP synthase subunit OSCP and the interaction of OSCP with Aβ peptide in Alzheimer’s disease patients and mouse models lead to F1FO-ATP synthase deregulation and disruption of synaptic mitochondrial function.