Publication: Inflammatory risk factors and pathologies promoting
Alzheimer’s disease progression: is RAGE the key?
Authors
Matrone, Carmela ; Djellou, Mehdi ; Taglialatela, Giulio ; Perrone, Lorena
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
https://doi.org/10.14670/HH-30.125
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info:eu-repo/semantics/article
Description
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.
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Citation
Histology and Histopathology, Vol. 30, n.º 2 (2015)
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