Autor: |
Schmidt AM; 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, Sahagan B, Nelson RB, Selmer J, Rothlein R, Bell JM |
Jazyk: |
angličtina |
Zdroj: |
Current opinion in investigational drugs (London, England : 2000) [Curr Opin Investig Drugs] 2009 Jul; Vol. 10 (7), pp. 672-80. |
Abstrakt: |
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. |
Databáze: |
MEDLINE |
Externí odkaz: |
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