title: Alcohol enhances Abeta42-induced neuronal cell death through mitochondrial dysfunction.
abstract: Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-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 Abeta-induced neuronal cell death. Abeta-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 Abeta-induced neuronal cell death. Our study shows that alcohol consumption enhances Abeta-induced neuronal cell death by increasing ROS and mitochondrial dysfunction.
authors.affiliation: Department of Anatomy and Cell biology, College of Medicine, Chung-Ang University, Seoul 156-756, Republic of Korea.
authors.forename: Do Yeon
authors.initials: DY
authors.lastname: Lee
authors.forename: Kyu-Sun
authors.initials: KS
authors.lastname: Lee
authors.forename: Hyun Jung
authors.initials: HJ
authors.lastname: Lee
authors.forename: Hee-Yeon
authors.initials: HY
authors.lastname: Jung
authors.forename: Jun Young
authors.initials: JY
authors.lastname: Lee
authors.forename: Sang Hyung
authors.initials: SH
authors.lastname: Lee
authors.forename: Young Chul
authors.initials: YC
authors.lastname: Youn
authors.forename: Kyung Mook
authors.initials: KM
authors.lastname: Seo
authors.forename: Jang Han
authors.initials: JH
authors.lastname: Lee
authors.forename: Won Bok
authors.initials: WB
authors.lastname: Lee
authors.forename: Sung Su
authors.initials: SS
authors.lastname: Kim
mesh_terms: D000544:Alzheimer Disease / Q000139:chemically induced* / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism* / Q000494:pharmacology; D017209:Apoptosis; D045744:Cell Line, Tumor; D000431:Ethanol / Q000633:toxicity*; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects / Q000235:genetics; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D016376:Oligonucleotides, Antisense / Q000235:genetics; D018384:Oxidative Stress; D010446:Peptide Fragments / Q000378:metabolism* / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016376:Oligonucleotides, Antisense; D010446:Peptide Fragments; D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; C075222:amyloid beta-protein (1-42); D000431:Ethanol; D051057:Proto-Oncogene Proteins c-akt