| AGEs/RAGE complex upregulates BACE1 via NF-κB pathway activation. | |
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MedLine Citation:
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PMID: 20638753 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Although the pathogenesis of sporadic Alzheimer disease (AD) is not clearly understood, it is likely dependent on several age-related factors. Diabetes is a risk factor for AD, and multiple mechanisms connecting the 2 diseases have been proposed. Hyperglycemia enhances the formation of advanced glycation end products (AGEs) that result from the auto-oxidation of glucose and fructose. The interaction of AGEs with their receptor, named RAGE, elicits the formation of reactive oxygen species that are also believed to be an early event in AD pathology. To investigate a functional link between the disorders diabetes and AD, the effect of 2 AGEs, pentosidine and glyceraldehydes-derived pyridinium (GLAP), was studied on BACE1 expression both in vivo, in streptozotocin treated rats, and in vitro in differentiated neuroblastoma cells. We showed that pentosidine and GLAP were able to upregulate BACE1 expression through their binding with RAGE and the consequent activation of NF-κB. In addition, both pentosidine and GLAP were found to be increased in the brain in sporadic AD patients. Our findings demonstrate that activation of the AGEs/RAGE axis, by upregulating the key enzyme for amyloid-β production, provides a pathologic link between diabetes mellitus and AD. |
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Authors:
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Michela Guglielmotto; Manuela Aragno; Elena Tamagno; Ilenia Vercellinatto; Sonia Visentin; Claudio Medana; Maria Graziella Catalano; Mark A Smith; George Perry; Oliviero Danni; Giuseppe Boccuzzi; Massimo Tabaton |
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Publication Detail:
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Type: Journal Article Date: 2010-07-17 |
Journal Detail:
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Title: Neurobiology of aging Volume: 33 ISSN: 1558-1497 ISO Abbreviation: Neurobiol. Aging Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2011-11-21 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8100437 Medline TA: Neurobiol Aging Country: United States |
Other Details:
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Languages: eng Pagination: 196.e13-27 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Experimental Medicine and Oncology, University of Turin, Turin, Italy. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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