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Curr Opin Investig Drugs. 2009 Jul;10(7):672-80.

The role of RAGE in amyloid-beta peptide-mediated pathology in Alzheimer's disease.

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1
Columbia University, College of Physicians and Surgeons, Department of Surgery, 630 West 168th Street, P&S 17-401, New York, NY 10032, USA. ams11@columbia.edu

Abstract

This review discusses current knowledge of the complex interactions between amyloid-beta (A beta) peptide, the receptor for advanced glycation endproducts (RAGE), and inflammatory mediators, focusing on the roles of such interactions in the pathogenesis of Alzheimer's disease. As a ubiquitous cell-surface receptor, RAGE demonstrates enhanced expression in an A beta-rich environment; the effects of RAGE on microglia, the blood-brain barrier and neurons are mediated through various signaling pathways. Relevant preclinical models illustrate that the A beta-RAGE interaction amplifies neuronal stress and the accumulation of A beta, impairs memory and learning, and exaggerates neuroinflammation. These findings suggest that RAGE may mediate a common proinflammatory pathway in neurodegenerative disorders.

PMID:
19579173
[Indexed for MEDLINE]
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