Acute high glucose exposure impairs synaptosomal vesicle release activity

The present work demonstrates that hyperglycemia can impair synaptic vesicular exocytosis, partially by reducing V-ATPase assembly. We hypothesize that these molecular changes can be a shared mechanistic contributor to synaptic dysfunction in AD and diabetes. Further studies are needed to investigate the impact of chronic hyperglycemia and glycolytic metabolism on synaptic vesicular activity and V-ATPase function in animal models of AD and diabetes.