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RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease.

Authors: Yan, SD  Chen, X  Fu, J  Chen, M  Zhu, H  Roher, A  Slattery, T  Zhao, L  Nagashima, M  Morser, J  Migheli, A  Nawroth, P  Stern, D  Schmidt, AM 
Citation: Yan SD, etal., Nature 1996 Aug 22;382(6593):685-91.
Pubmed: (View Article at PubMed) PMID:8751438
DOI: Full-text: DOI:10.1038/382685a0

Amyloid-beta peptide is central to the pathology of Alzheimer's disease, because it is neurotoxic--directly by inducing oxidant stress, and indirectly by activating microglia. A specific cell-surface acceptor site that could focus its effects on target cells has been postulated but not identified. Here we present evidence that the 'receptor for advanced glycation end products' (RAGE) is such a receptor, and that it mediates effects of the peptide on neurons and microglia. Increased expressing of RAGE in Alzheimer's disease brain indicates that it is relevant to the pathogenesis of neuronal dysfunction and death.


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CRRD Object Information
CRRD ID: 1300365
Created: 2004-07-20
Species: All species
Last Modified: 2004-07-20
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.