Alcohol enhances Aβ42-induced neuronal cell death through mitochondrial dysfunction
Abstract
Mitochondrial dysfunction is a hallmark of beta-amyloid (Aβ)-induced neuronal toxicity in Alzheimer’s disease (AD). Epidemiological studies have indicated that alcohol consumption plays a role in the development of AD. Here we show that alcohol exposure has a synergistic effect on Aβ-induced neuronal cell death. Aβ-treated cultured neurons displayed spontaneous generation of reactive oxygen species (ROS), disruption of their mitochondrial membrane potential, induction of caspase-3 and p53 activities, and loss of cell viability. Alcohol exposure facilitated Aβ-induced neuronal cell death. Our study shows that alcohol consumption enhances Aβ-induced neuronal cell death by increasing ROS and mitochondrial dysfunction.
Keywords: Alzheimer’s disease, Aβ, Ethanol, Mitochondria, ROS
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PII: S0014-5793(08)00907-1
doi:10.1016/j.febslet.2008.11.007
© 2008 Federation of European Biochemical Societies. Published by Elsevier BV. All rights reserved.
