Cutting Calories Shields
Brain Cells From Effects
Of Aging
By Amy Norton
NEW YORK (Reuters Health) - While low-calorie diets have been linked to a longer lifespan in both animals and humans, the reason for the association has been unclear. Now researchers have evidence from studies in mice that cutting calories shields brain cells from the decline that comes with aging.
According to investigators at the University of Wisconsin-Madison, the study suggests that calorie intake may help determine a person's risk for degenerative brain diseases like Alzheimer's and Parkinson's disease.
Cheol-Koo Lee and his colleagues report their findings in the July issue of Nature Genetics. In experiments with mice, Lee's team used a gene chip, a new type of gene-scanning technology, to rapidly determine the activity of more than 6,000 genes in the animals' brain tissue.
The researchers found that aging boosted the activity of some genes and decreased it in others. As the mice aged, activity increased in genes responsible for inflammation and the stress response--two key factors related to cell damage. In addition, activity declined in genes involved in repairing cell damage. Co-investigator Dr. Richard Weindruch told Reuters Health that inflammation in the brain is believed to be related to certain diseases such as Alzheimer's.
Since it is known that animals live longer on restricted diets, Weindruch said, his team expected that brain tissue from mice raised on low-calorie diets would show fewer aging-related gene shifts. The researchers had previously shown this to be true in mouse skeletal muscle.
Indeed, when Weindruch and his colleagues compared elderly mice raised on a low-calorie diet with those on a standard diet, they found the calorie-deprived mice had maintained a more youthful balance of gene activity.
Exactly how calorie intake affects genes over a lifetime is unknown, according to Weindruch. He said it is possible that restricting energy intake results in basic changes in energy metabolism, which in turn helps regulate gene activity.
Weindruch also noted that a study in Parkinson's patients has suggested that high calorie intake contributes to the risk for the disease. ``These findings,'' he said, ``provide a link at the molecular level.''
SOURCE: Nature Genetics 2000;25:294-297.
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