Aβ initiates brain hypometabolism, network dysfunction and behavioral abnormalities via NOX2-induced oxidative stress in mice

Abstract

Anton Malkov, Irina Popova et al. demonstrate that beta-amyloid application induces oxidative stress and reduces glucose consumption in the mouse brain, leading to network hyperactivity and behavioral changes—pathologies similar to those observed early on in Alzheimer’s disease patients. Inhibition of NADPH oxidase 2 (NOX2) rescued these phenotypes, suggesting that NOX2 may represent an important therapeutic target for Alzheimer’s disease.