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dc.contributor.authorYan, Shirley ShiDu
dc.contributor.authorBierhaus, Angelika
dc.contributor.authorNawroth, Peter P.
dc.contributor.authorStern, David M.
dc.date.accessioned2014-07-22T15:53:05Z
dc.date.available2014-07-22T15:53:05Z
dc.date.issued2009-04
dc.identifier.citationYan, Shirley ShiDu et al. (2009). RAGE and Alzheimer’s Disease: A Progression Factor for Amyloid-β-Induced Cellular Perturbation? Journal of Alzheimer's Disease 16(4):833-843.
dc.identifier.issn1387-2877
dc.identifier.urihttp://hdl.handle.net/1808/14813
dc.descriptionThis is the publisher's version, also available electronically from http://iospress.metapress.com/content/d6621608n32478r2/?genre=article&issn=1387-2877&volume=16&issue=4&spage=833
dc.description.abstractReceptor for Advanced Glycation Endproducts (RAGE) is a multiligand member of the immunoglobulin superfamily of cell surface molecules which serves as a receptor for amyloid-β peptide (Aβ) on neurons, microglia, astrocytes, and cells of vessel wall. Increased expression of RAGE is observed in regions of the brain affected by Alzheimer's disease (AD), and Aβ-RAGE interaction in vitro leads to cell stress with the generation of reactive oxygen species and activation of downstream signaling mechanisms including the MAP kinase pathway. RAGE-mediated activation of p38 MAP kinase in neurons causes Aβ-induced inhibition of long-term potentiation in slices of entorhinal cortex. Increased expression of RAGE in an Aβ-rich environment, using transgenic mouse models, accelerates and accentuates pathologic, biochemical, and behavioral abnormalities compared with mice overexpressing only mutant amyloid-β protein precursor. Interception of Aβ interaction with RAGE, by infusion of soluble RAGE, decreases Aβ content and amyloid load, as well as improving learning/memory and synaptic function, in a murine transgenic model of Aβ accumulation. These data suggest that RAGE may be a therapeutic target for AD.
dc.publisherIOS Press
dc.relation.isversionofhttp://iospress.metapress.com/content/d6621608n32478r2/?genre=article&issn=1387-2877&volume=16&issue=4&spage=833
dc.subjectAmyloid-β peptide receptor
dc.subjectCerebral blood flow
dc.subjectendothelin-1
dc.subjectImmunoglobulin superfamily
dc.subjectLong-term potentiation
dc.subjecttransgenic model
dc.titleRAGE and Alzheimer’s Disease: A Progression Factor for Amyloid-β-Induced Cellular Perturbation?
dc.typeArticle
kusw.kuauthorYan, Shirley ShiDu
kusw.kudepartmentPharmacology and Toxicology
kusw.oastatusfullparticipation
kusw.oaversionScholarly/refereed, publisher version
kusw.oapolicyThis item meets KU Open Access policy criteria.
dc.rights.accessrightsopenAccess


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