RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1996-08

AUTHORS

Shi Du Yan, Xi Chen, Jin Fu, Ming Chen, Huaijie Zhu, Alex Roher, Timothy Slattery, Lei Zhao, Mariko Nagashima, John Morser, Antonio Migheli, Peter Nawroth, David Stern, Ann Marie Schmidt

ABSTRACT

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 expression of RAGE in Alzheimer's disease brain indicates that it is relevant to the pathogenesis of neuronal dysfunction and death. More... »

PAGES

685-691

Journal

TITLE

Nature

ISSUE

6593

VOLUME

382

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/382685a0

    DOI

    http://dx.doi.org/10.1038/382685a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1012543542

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/8751438


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    curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1038/382685a0'

    RDF/XML is a standard XML format for linked data.

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