Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/67989
Title: Neuroprotective role of trans-resveratrol in a murine model of familial Alzheimer's disease 
Author: Porquet Costa, David
Griñán Ferré, Christian
Ferrer, Isidro (Ferrer Abizanda)
Camins Espuny, Antoni
Sanfeliu i Pujol, Coral
Valle i Macià, Jaume del
Pallàs i Llibería, Mercè, 1964-
Keywords: Malaltia d'Alzheimer
Mitocondris
Malalties neurodegeneratives
Polifenols
Alzheimer's disease
Mitochondria
Neurodegenerative Diseases
Polyphenols
Issue Date: 10-Oct-2014
Publisher: IOS Press
Abstract: The amyloid-β protein precursor/presenilin 1 (AβPP/PS1) mouse model of Alzheimer's disease (AD) has provided robust neuropathological hallmarks of familial AD-like pattern. AD is a neurodegenerative process that causes severe cognitive impairment; it is characterized by the accumulation of amyloid-β (Aβ) and hyperphosphorylated tau forms and by oxidative and inflammatory processes in brain. Currently, efforts are made to understand biochemical pathways because there is no effective therapy for AD. Resveratrol is a polyphenol that induces expression and activation of several neuroprotective pathways involving Sirtuin1 and AMPK. The objective of this work was to assess the effect of oral resveratrol administration on AβPP/PS1 mice. Long-term resveratrol treatment significantly prevented memory loss as measured by the object recognition test. Moreover, resveratrol reduced the amyloid burden and increased mitochondrial complex IV protein levels in mouse brain. These protective effects of resveratrol were mainly mediated by increased activation of Sirtuin 1 and AMPK pathways in mice. However, an increase has been observed in IL1β and TNF gene expression, indicating that resveratrol promoted changes in inflammatory processes, although no changes were detected in other key actors of the oxidative stress pathway. Taken together, our findings suggest that resveratrol is able to reduce the harmful process that occurs in AβPP/PS1 mouse hippocampus, preventing memory loss.
Note: Reproducció del document publicat a: http://dx.doi.org/10.3233/JAD-140444
It is part of: Journal of Alzheimer's Disease, 2014, vol. 42, num. 4, p. 1209-1220
Related resource: http://dx.doi.org/10.3233/JAD-140444
URI: http://hdl.handle.net/2445/67989
ISSN: 1387-2877
Appears in Collections:Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
Articles publicats en revistes (Patologia i Terapèutica Experimental)

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