Alcohol enhances A beta 42-induced neuronal cell death through mitochondrial dysfunction
- Authors
- Lee, Do Yeon; Lee, Kyu-Sun; Lee, Hyun Jung; Jung, Hee-Yeon; Lee, Jun Young; Lee, Sang Hyung; Youn, Young Chul; Seo, Kyung Mook; Lee, Jang Han; Lee, Won Bok; Kim, 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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- Appears in
Collections - College of Social Sciences > Department of Psychology > 1. Journal Articles
- College of Medicine > College of Medicine > 1. Journal Articles
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