The S100B/RAGE Axis in Alzheimer's Disease

Increasing evidence suggests that the small EF-hand calcium-binding protein S100B plays an important role in Alzheimer's disease. Among other evidences are the increased levels of both S100B and its receptor, the Receptor for Advanced Glycation Endproducts (RAGEs) in the AD diseased brain. The...

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Detalles Bibliográficos
Autores principales: Leclerc, Estelle, Sturchler, Emmanuel, Vetter, Stefan W.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2010
Materias:
Review Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905692/
https://www.ncbi.nlm.nih.gov/pubmed/20672051
http://dx.doi.org/10.1155/2010/539581
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author Leclerc, Estelle
Sturchler, Emmanuel
Vetter, Stefan W.
author_facet Leclerc, Estelle
Sturchler, Emmanuel
Vetter, Stefan W.
author_sort Leclerc, Estelle
collection PubMed
description Increasing evidence suggests that the small EF-hand calcium-binding protein S100B plays an important role in Alzheimer's disease. Among other evidences are the increased levels of both S100B and its receptor, the Receptor for Advanced Glycation Endproducts (RAGEs) in the AD diseased brain. The regulation of RAGE signaling by S100B is complex and probably involves other ligands including the amyloid beta peptide (Aβ), the Advanced Glycation Endproducts (AGEs), or transtheyretin. In this paper we discuss the current literature regarding the role of S100B/RAGE activation in Alzheimer's disease.
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spelling pubmed-29056922010-07-29 The S100B/RAGE Axis in Alzheimer's Disease Leclerc, Estelle Sturchler, Emmanuel Vetter, Stefan W. Cardiovasc Psychiatry Neurol Review Article Increasing evidence suggests that the small EF-hand calcium-binding protein S100B plays an important role in Alzheimer's disease. Among other evidences are the increased levels of both S100B and its receptor, the Receptor for Advanced Glycation Endproducts (RAGEs) in the AD diseased brain. The regulation of RAGE signaling by S100B is complex and probably involves other ligands including the amyloid beta peptide (Aβ), the Advanced Glycation Endproducts (AGEs), or transtheyretin. In this paper we discuss the current literature regarding the role of S100B/RAGE activation in Alzheimer's disease. Hindawi Publishing Corporation 2010 2010-06-21 /pmc/articles/PMC2905692/ /pubmed/20672051 http://dx.doi.org/10.1155/2010/539581 Text en Copyright © 2010 Estelle Leclerc et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Leclerc, Estelle
Sturchler, Emmanuel
Vetter, Stefan W.
The S100B/RAGE Axis in Alzheimer's Disease
title The S100B/RAGE Axis in Alzheimer's Disease
title_full The S100B/RAGE Axis in Alzheimer's Disease
title_fullStr The S100B/RAGE Axis in Alzheimer's Disease
title_full_unstemmed The S100B/RAGE Axis in Alzheimer's Disease
title_short The S100B/RAGE Axis in Alzheimer's Disease
title_sort s100b/rage axis in alzheimer's disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905692/
https://www.ncbi.nlm.nih.gov/pubmed/20672051
http://dx.doi.org/10.1155/2010/539581
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