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| pubmed-article:15834426 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:15834426 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:15834426 | lifeskim:mentions | umls-concept:C1880371 | lld:lifeskim |
| pubmed-article:15834426 | lifeskim:mentions | umls-concept:C1176299 | lld:lifeskim |
| pubmed-article:15834426 | lifeskim:mentions | umls-concept:C0205198 | lld:lifeskim |
| pubmed-article:15834426 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:15834426 | pubmed:dateCreated | 2005-5-5 | lld:pubmed |
| pubmed-article:15834426 | pubmed:abstractText | Increased Abeta42 production has been linked to the development of Alzheimer disease. We now identify a number of compounds that raise Abeta42. Among the more potent Abeta42-raising agents identified are fenofibrate, an antilipidemic agent, and celecoxib, a COX-2-selective NSAID. Many COX-2-selective NSAIDs tested raised Abeta42, including multiple COX-2-selective derivatives of two Abeta42-lowering NSAIDs. Compounds devoid of COX activity and the endogenous isoprenoids FPP and GGPP also raised Abeta42. These compounds seem to target the gamma-secretase complex, increasing gamma-secretase-catalyzed production of Abeta42 in vitro. Short-term in vivo studies show that two Abeta42-raising compounds increase Abeta42 levels in the brains of mice. The elevations in Abeta42 by these compounds are comparable to the increases in Abeta42 induced by Alzheimer disease-causing mutations in the genes encoding amyloid beta protein precursor and presenilins, raising the possibility that exogenous compounds or naturally occurring isoprenoids might increase Abeta42 production in humans. | lld:pubmed |
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| pubmed-article:15834426 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15834426 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15834426 | pubmed:month | May | lld:pubmed |
| pubmed-article:15834426 | pubmed:issn | 1078-8956 | lld:pubmed |
| pubmed-article:15834426 | pubmed:author | pubmed-author:DasPritamP | lld:pubmed |
| pubmed-article:15834426 | pubmed:author | pubmed-author:GoldeTodd ETE | lld:pubmed |
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| pubmed-article:15834426 | pubmed:author | pubmed-author:KukarThomasT | lld:pubmed |
| pubmed-article:15834426 | pubmed:author | pubmed-author:KooEdward HEH | lld:pubmed |
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| pubmed-article:15834426 | pubmed:author | pubmed-author:SagiSarah ASA | lld:pubmed |
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| pubmed-article:15834426 | pubmed:author | pubmed-author:BeardJennyJ | lld:pubmed |
| pubmed-article:15834426 | pubmed:author | pubmed-author:MeritSamiS | lld:pubmed |
| pubmed-article:15834426 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15834426 | pubmed:volume | 11 | lld:pubmed |
| pubmed-article:15834426 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15834426 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15834426 | pubmed:pagination | 545-50 | lld:pubmed |
| pubmed-article:15834426 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:15834426 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15834426 | pubmed:articleTitle | Diverse compounds mimic Alzheimer disease-causing mutations by augmenting Abeta42 production. | lld:pubmed |
| pubmed-article:15834426 | pubmed:affiliation | Department of Neuroscience, Mayo Clinic, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, Florida 32224, USA. | lld:pubmed |
| pubmed-article:15834426 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15834426 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:15834426 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15834426 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:15834426 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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