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RAGE and Alzheimer’s Disease: A Progression Factor for Amyloid-β-Induced Cellular Perturbation?
dc.contributor.author | Yan, Shirley ShiDu | |
dc.contributor.author | Bierhaus, Angelika | |
dc.contributor.author | Nawroth, Peter P. | |
dc.contributor.author | Stern, David M. | |
dc.date.accessioned | 2014-07-22T15:53:05Z | |
dc.date.available | 2014-07-22T15:53:05Z | |
dc.date.issued | 2009-04 | |
dc.identifier.citation | Yan, 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.issn | 1387-2877 | |
dc.identifier.uri | http://hdl.handle.net/1808/14813 | |
dc.description | This 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.abstract | Receptor 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.publisher | IOS Press | |
dc.relation.isversionof | http://iospress.metapress.com/content/d6621608n32478r2/?genre=article&issn=1387-2877&volume=16&issue=4&spage=833 | |
dc.subject | Amyloid-β peptide receptor | |
dc.subject | Cerebral blood flow | |
dc.subject | endothelin-1 | |
dc.subject | Immunoglobulin superfamily | |
dc.subject | Long-term potentiation | |
dc.subject | transgenic model | |
dc.title | RAGE and Alzheimer’s Disease: A Progression Factor for Amyloid-β-Induced Cellular Perturbation? | |
dc.type | Article | |
kusw.kuauthor | Yan, Shirley ShiDu | |
kusw.kudepartment | Pharmacology and Toxicology | |
kusw.oastatus | fullparticipation | |
kusw.oaversion | Scholarly/refereed, publisher version | |
kusw.oapolicy | This item meets KU Open Access policy criteria. | |
dc.rights.accessrights | openAccess |
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Pharmacy Scholarly Works [299]