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Alcohol enhances A beta 42-induced neuronal cell death through mitochondrial dysfunction

Authors
Lee, Do YeonLee, Kyu-SunLee, Hyun JungJung, Hee-YeonLee, Jun YoungLee, Sang HyungYoun, Young ChulSeo, Kyung MookLee, Jang HanLee, Won BokKim, Sung Su
Issue Date
Dec-2008
Publisher
WILEY
Keywords
Alzheimer's disease; A beta; Ethanol; Mitochondria; ROS
Citation
FEBS LETTERS, v.582, no.30, pp 4185 - 4190
Pages
6
Journal Title
FEBS LETTERS
Volume
582
Number
30
Start Page
4185
End Page
4190
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23503
DOI
10.1016/j.febslet.2008.11.007
ISSN
1873-3468
1873-3468
Abstract
Mitochondrial dysfunction is a hallmark of beta-amyloid (A beta)-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 A beta-induced neuronal cell death. A beta-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 A beta-induced neuronal cell death. Our study shows that alcohol consumption enhances A beta-induced neuronal cell death by increasing ROS and mitochondrial dysfunction. Crown Copyright (c) 2008 Published by Elsevier B. V. on behalf of the Federation of European Biochemical Societies. All rights reserved.
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사회과학대학 (심리학과)
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