An article published online on December 4 2003 in the journal of the Federation of the American Societies for Experimental Biology (FASEB http://www.fasebj.org/ ), detailed the findings of researchers from the University of Pennsylvania that vitamin E supplemented early in life is effective in reducing amyloid-beta levels and amyloid deposition in a mouse model of Alzheimer’s disease (AD). Amyloid-beta is a peptide that accumulates as plaque in the brains of individuals with Alzheimer’s disease. The protective benefit of vitamin E supplementation was found when vitamin E was started early in life.
Mice bred to develop amyloid-beta deposits received diets supplemented with vitamin E or a placebo starting at five months of age until the age of thirteen months. In a second experiment, the mice received the vitamin or a placebo from the age of fourteen months until the age of twenty months.
At the conclusion of the experiments, brain lipid peroxidation was found to be reduced in the mice receiving vitamin E compared to the placebo groups. The mice receiving the vitamin from five to thirteen months experienced a significant reduction in amyloid-beta levels and amyloid-beta deposition compared to the placebo group who experienced amyloid-beta levels and deposition consistent with their age. In the second experiment, older mice receiving vitamin E did not did not differ in regard to amyloid-beta compared to the control group.
Because vitamin E suppresses lipid peroxidation, and because oxidative stress has been shown to be increased in Alzheimer’s disease, vitamin E may help to prevent the disease due to its antioxidant ability, however it evidently needs to be started early, before amyloid plaques have been deposited. The authors conclude that, “any therapeutic strategy aimed at targeting oxidative stress should be initiated at the earliest possible state of the disease, ideally in subjects at high risk for developing AD.” (Sung S, et al, “Early vitamin E supplementiton in young but not aged mice reduces AB levels and amyloid deposition in a transgenic model of Alzheimer’s disease,” FASEB, December 4 2003.)
Source: Life Extension Magazine – Weekly Update December 30, 2003.