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Review
. 2008 Dec 3;9 Suppl 2(Suppl 2):S6.
doi: 10.1186/1471-2202-9-S2-S6.

Therapeutic potential of resveratrol in Alzheimer's disease

Valérie Vingtdeux  1 , Ute Dreses-Werringloer, Haitian Zhao, Peter Davies, Philippe Marambaud
Affiliations
Review

Therapeutic potential of resveratrol in Alzheimer's disease

Valérie Vingtdeux et al. BMC Neurosci. .

Abstract

Several epidemiological studies indicate that moderate consumption of red wine is associated with a lower incidence of dementia and Alzheimer's disease. Red wine is enriched in antioxidant polyphenols with potential neuroprotective activities. Despite scepticism concerning the bioavailability of these polyphenols, in vivo data have clearly demonstrated the neuroprotective properties of the naturally occurring polyphenol resveratrol in rodent models for stress and diseases. Furthermore, recent work in cell cultures and animal models has shed light on the molecular mechanisms potentially involved in the beneficial effects of resveratrol intake against the neurodegenerative process in Alzheimer's disease.

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Figures

Figure 1
Figure 1
Schematic representation of the plasminogen system. The proenzyme plasminogen (Plg) is converted to the active serine protease plasmin (Plm) by the soluble or membrane bound urokinase-type plasminogen activator (u-PA). Membrane bound u-PA binds to a cellular u-PA receptor (u-PAR). Inhibition of the plasminogen system may occur at the level of the plasminogen activators by plasminogen activator inhibitors (such as PAI-1), or at the level of plasmin by α2-plasmin inhibitor (α2-PI) (also called α2-antiplasmin (α2AP)).
See this image and copyright information in PMC

References

    1. Selkoe DJ. Alzheimer's disease: genes, proteins, and therapy. Physiol Rev. 2001;81:741–766. - PubMed
    1. Davies P. A very incomplete comprehensive theory of Alzheimer's disease. Ann N Y Acad Sci. 2000;924:8–16. doi: 10.1111/j.1749-6632.2000.tb05553.x. - DOI - PubMed
    1. Goedert M, Spillantini MG. Tau mutations in frontotemporal dementia FTDP-17 and their relevance for Alzheimer's disease. Biochim Biophys Acta. 2000;1502:110–121. - PubMed
    1. Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science. 2002;297:353–356. doi: 10.1126/science.1072994. - DOI - PubMed
    1. Marambaud P, Robakis NK. Genetic and molecular aspects of Alzheimer's disease shed light on new mechanisms of transcriptional regulation. Genes Brain Behav. 2005;4:134–146. doi: 10.1111/j.1601-183X.2005.00086.x. - DOI - PubMed

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