rdf:type |
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lifeskim:mentions |
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pubmed:issue |
15
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pubmed:dateCreated |
2002-10-23
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pubmed:abstractText |
Amyloid beta peptide (Abeta) is a neurotoxic metabolic product of the amyloid precursor protein (APP). Abeta is strongly implicated in the pathology of Alzheimer's disease (AD) and can be formed intracellularly. In this study, we show that the addition of Abeta to isolated mouse brain mitochondria can directly induce cytochrome c (Cyt c) release and mitochondrial swelling, which were partially inhibited by cyclosporin A (CsA). These results suggest that the Abetaaccumulated intracellularly by APP processing might exert neurotoxicity by interacting with mitochondria and inducing mitochondrial swelling and release of Cyt c, which activates caspase-3 and finally can lead to apoptosis in neuronal cells and to neurodegeneration in AD.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/CASP3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Casp3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Cytochrome c Group,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-42)
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0959-4965
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pubmed:author |
pubmed-author:ChangKeun-AKA,
pubmed-author:ChoiSe-HoonSH,
pubmed-author:JeongSung-JinSJ,
pubmed-author:KimEun-MeeEM,
pubmed-author:KimHye-SunHS,
pubmed-author:LeeJean-PyoJP,
pubmed-author:LeeJun-HoJH,
pubmed-author:ParkCheol HyoungCH,
pubmed-author:SeoJi-HeuiJH,
pubmed-author:SuhYoo-HunYH,
pubmed-author:WittendorpM CMC
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pubmed:issnType |
Print
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pubmed:day |
28
|
pubmed:volume |
13
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1989-93
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:12395106-Alzheimer Disease,
pubmed-meshheading:12395106-Amyloid beta-Peptides,
pubmed-meshheading:12395106-Animals,
pubmed-meshheading:12395106-Apoptosis,
pubmed-meshheading:12395106-Brain,
pubmed-meshheading:12395106-Calcium Signaling,
pubmed-meshheading:12395106-Caspase 3,
pubmed-meshheading:12395106-Caspases,
pubmed-meshheading:12395106-Cell Membrane Permeability,
pubmed-meshheading:12395106-Cells, Cultured,
pubmed-meshheading:12395106-Cyclosporine,
pubmed-meshheading:12395106-Cytochrome c Group,
pubmed-meshheading:12395106-Enzyme Inhibitors,
pubmed-meshheading:12395106-Humans,
pubmed-meshheading:12395106-Mice,
pubmed-meshheading:12395106-Mitochondria,
pubmed-meshheading:12395106-Neurons,
pubmed-meshheading:12395106-Peptide Fragments
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pubmed:year |
2002
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pubmed:articleTitle |
Amyloid beta peptide induces cytochrome C release from isolated mitochondria.
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pubmed:affiliation |
Department of Pharmacology, College of Medicine, National Creative Research Initiative Center for Alzheimer's Dementia and Neuroscience Research Institute, MRC, Seoul National University, Seoul 110-799, South Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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