Alcohol enhances Abeta42-induced neuronal cell death through mitochondrial dysfunction

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dc.contributor.authorD Y Lee-
dc.contributor.authorKyu-Sun Lee-
dc.contributor.authorH J Lee-
dc.contributor.authorH Y Jung-
dc.contributor.authorJ Y Lee-
dc.contributor.authorS H Lee-
dc.contributor.authorY C Youn-
dc.contributor.authorK M Seo-
dc.contributor.authorJ H Lee-
dc.contributor.authorW B Lee-
dc.contributor.authorS S Kim-
dc.date.accessioned2017-04-19T09:12:26Z-
dc.date.available2017-04-19T09:12:26Z-
dc.date.issued2008-
dc.identifier.issn0014-5793-
dc.identifier.uri10.1016/j.febslet.2008.11.007ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8749-
dc.description.abstractMitochondrial 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.-
dc.publisherWiley-
dc.titleAlcohol enhances Abeta42-induced neuronal cell death through mitochondrial dysfunction-
dc.title.alternativeAlcohol enhances Abeta42-induced neuronal cell death through mitochondrial dysfunction-
dc.typeArticle-
dc.citation.titleFEBS Letters-
dc.citation.number30-
dc.citation.endPage4190-
dc.citation.startPage4185-
dc.citation.volume582-
dc.contributor.affiliatedAuthorKyu-Sun Lee-
dc.contributor.alternativeName이도연-
dc.contributor.alternativeName이규선-
dc.contributor.alternativeName이현정-
dc.contributor.alternativeName정희연-
dc.contributor.alternativeName이준영-
dc.contributor.alternativeName이상형-
dc.contributor.alternativeName윤용철-
dc.contributor.alternativeName서경묵-
dc.contributor.alternativeName이장한-
dc.contributor.alternativeName이원복-
dc.contributor.alternativeName김성수-
dc.identifier.bibliographicCitationFEBS Letters, vol. 582, no. 30, pp. 4185-4190-
dc.identifier.doi10.1016/j.febslet.2008.11.007-
dc.subject.keyword-
dc.subject.keywordAlzheimer's disease-
dc.subject.keywordEthanol-
dc.subject.keywordMitochondria-
dc.subject.keywordROS-
dc.subject.local-
dc.subject.localalzheimer's disease-
dc.subject.localAlzheimer’s disease (AD)-
dc.subject.localAlzheimer’s disease-
dc.subject.localAlzheimer's Disease-
dc.subject.localAlzheimer disease-
dc.subject.localAlzheimer's disease (AD)-
dc.subject.localAlzheimer′s disease-
dc.subject.localAlzheimer's disease-
dc.subject.localEthanol-
dc.subject.localETHANOL-
dc.subject.localethanol-
dc.subject.localMitochondria-
dc.subject.localmitochondria-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.description.journalClassY-
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