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September 19, 2006
A new study directed by Mount Sinai School of Medicine has found that moderate consumption of Cabernet Sauvignon red wine may help reduce the incidence of Alzheimer's Disease (AD). The study will be published in the November 2006 issue of The FASEB Journal.
"Our study is the first to report that moderate consumption of red wine in a form of Cabernet Sauvignon delivered in the drinking water for 7 months significantly reduces AD-type-amyloid neuropathology, and memory deterioration in 11-month-old transgenic mice that model AD," reported researchers Dr. Giulio Maria Pasinetti and Dr. Jun Wang at Mount Sinai.
"This study supports epidemiological evidence indicating that moderate wine consumption, within the range recommended by the FDA dietary guidelines of one drink per day for women and two for men, may help reduce the relative risk for AD clinical dementia."
The researchers say people with AD exhibit elevated levels of beta-amyloid peptides that cause plaque buildup in the brain, which is the main characteristic of Alzheimer's. An estimated 4.5 million Americans have AD. Presently, there are no known cures or effective preventive strategies.
While genetic factors are responsible in early-onset cases, they appear to play less of a role in late-onset-sporadic AD cases, the most common form of AD. However, lifestyle factors such as diet and now moderate wine consumption are receiving increasing attention for their potential preventative impact.
Using mice, researchers at Mount Sinai tested whether moderate consumption of the red wine Cabernet Sauvignon changes AD-type neuropathology and cognitive deterioration. The wine used was delivered in a final concentration of approximately 6 percent ethanol.
It was found that Cabernet Sauvignon significantly reduced AD-type deterioration of spatial memory function and A neuropathology in mice relative to control mice that were treated with either a comparable amount of ethanol or water alone. Cabernet Sauvignon was found to exert a beneficial effect by promoting non-amyloidogenic processing of amyloid precursor protein, which ultimately prevents the generation of AD-amyloid neuropathology.
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