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Alcohol enhances Aβ42‐induced neuronal cell death through mitochondrial dysfunction
Author(s) -
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
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.11.007
Subject(s) - programmed cell death , mitochondrion , reactive oxygen species , microbiology and biotechnology , apoptosis , viability assay , cell , caspase , oxidative stress , biology , chemistry , biochemistry
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.