Advanced

Inflammatory risk factors and pathologies promoting Alzheimer's disease progression: is RAGE the key?

Matrone, Carmela; Djelloul, Mehdi LU ; Taglialatela, Giulio and Perrone, Lorena (2015) In Histology and Histopathology 30(2). p.125-139
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... (More)
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 RAGE-induced inflammation as a risk pathway that is implicated in AD pathophysiology. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Histology and Histopathology
volume
30
issue
2
pages
125 - 139
publisher
Histology and Histopathology
external identifiers
  • pmid:25014735
  • wos:000351201300001
ISSN
1699-5848
language
English
LU publication?
yes
id
05a40e02-cdb8-4b9d-8d16-bbe9916d22a8 (old id 4582961)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25014735?dopt=Abstract
date added to LUP
2014-08-07 20:18:02
date last changed
2016-09-30 05:34:56
@article{05a40e02-cdb8-4b9d-8d16-bbe9916d22a8,
  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 RAGE-induced inflammation as a risk pathway that is implicated in AD pathophysiology.},
  author       = {Matrone, Carmela and Djelloul, Mehdi and Taglialatela, Giulio and Perrone, Lorena},
  issn         = {1699-5848},
  language     = {eng},
  number       = {2},
  pages        = {125--139},
  publisher    = {Histology and Histopathology},
  series       = {Histology and Histopathology},
  title        = {Inflammatory risk factors and pathologies promoting Alzheimer's disease progression: is RAGE the key?},
  volume       = {30},
  year         = {2015},
}