Longevinex® Bulletin:  Resveratrol Eradicates Brain Plaque Associated With Senility (animal study)

 

Researchers at the Weill Medical College of Cornell University report that dietary supplementation with the red wine molecule resveratrol (rez-vair-ah-trawl) dramatically reduces plaque formation in animal brains, surprisingly without activating the Sirtuin1 gene. 

 

Oral resveratrol produced large reductions in brain plaque in the hypothalamus (-90%), striatum (-89%), and medial cortex (-48%) sections of the brain.  Previously, studies had shown that direct injection of resveratrol into brain tissues reduces degeneration and prevents learning impairment.  This study shows that oral doses of resveratrol may reduce beta amyloid plaque associated with aging changes in the brain.  Researchers theorize that one mechanism for plaque eradication is the ability of resveratrol to chelate (remove) copper.  [Neurochemistry International, Nov. 8, 2008 early online]

 

 

 

 

 

 

Plaque counts

 

 

 

 

Percent plaque area

 

 

 

 

 

 

Abstract:  Neurochemistry International   2008 Nov 8. [Epub ahead of print]

Dietary supplementation with resveratrol reduces plaque pathology in a transgenic model of Alzheimer's disease.

Karuppagounder  SS, Pinto JT, Xu  H, Chen LH, Beal  MF, Gibson GE.

Department of Neurology and Neurosciences, Weill Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Ave., White Plains, NY 10605, United States.

Resveratrol, a polyphenol found in red wine, peanuts, soy beans, and pomegranates, possesses a wide range of biological effects. Since resveratrol's properties seem ideal for treating neurodegenerative diseases, its ability to diminish amyloid plaques was tested. Mice were fed clinically feasible dosages of resveratrol for forty-five days. Neither resveratrol nor its conjugated metabolites were detectable in brain. Nevertheless, resveratrol diminished plaque formation in a region specific manner. The largest reductions in the percent area occupied by plaques were observed in medial cortex (-48%), striatum (-89%) and hypothalamus (-90%). The changes occurred without detectable activation of SIRT-1 or alterations in APP processing. However, brain glutathione declined 21% and brain cysteine increased 54%. The increased cysteine and decreased glutathione may be linked to the diminished plaque formation. This study supports the concept that onset of neurodegenerative disease may be delayed or mitigated with use of dietary chemo-preventive agents that protect against beta-amyloid induced neuronal damage.