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Title: Inflammatory risk factors and pathologies promoting Alzheimer’s disease progression: is RAGE the key?
Issue Date: 2015
Publisher: F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
Citation: Histology and Histopathology, Vol. 30, n.º 2 (2015)
ISSN: 1699-5848
Related subjects: CDU::5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citología
Keywords: Alzheimer Disease
Risk factors
Abstract: Epidemiological studies reveal growing evidence that most cases of Alzheimer’s Disease (AD) likely involve a combination of genetic and environmental risk factors. Identifying and validating these risk factors remains one of the most critical scientific challenges. Several diseases appear to have strong implications for neurodegeneration leading to dementia. This risk encompasses different forms of cardiovascular disease, carotid atherosclerosis, history of hypertension or high cholesterol, Type II diabetes, stroke or transient ischemic attack and brain trauma. However, the molecular pathways that are common and central in the progression of these diseases and AD are not yet elucidated. Unveiling these critical mechanisms at the molecular level is necessary for the development of therapeutic strategies aimed at preventing AD progression. The Receptor for Advanced Glycation Endproducts (RAGE) plays a key role in all the diseases that represent a risk for AD. RAGE-mediated signaling also contributes to neurodegeneration in AD, suggesting that it may mediate the effect of risk factors in promoting AD. We will summarize the current knowledge on the role of RAGE in pathologies promoting AD and in AD progression. We will also provide evidence showing the relevance of RAGEinduced inflammation as a risk pathway that is implicated in AD pathophysiology.
Primary author: Matrone, Carmela
Djellou, Mehdi
Taglialatela, Giulio
Perrone, Lorena
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 15
Rights: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 International
Appears in Collections:Vol.30, nº2 (2015)

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