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Accelerated Aging Gene Found in Mice - 2001-11-07


Researchers have identified a gene that triggers accelerated aging in mice. While the gene is not thought to be the only one responsible for aging, its discovery adds another clue to the mystery of why we grow old.

No one knows why some animals live longer than others. But researchers recently discovered a cluster of genes in very old people, those who are age 90 or older, which appears to be responsible for longevity.

Now, scientists at the U.S. National Heart, Lung and Blood Institute have discovered a gene that can cut life span by causing premature aging.

The gene makes an enzyme, called methionine sulfoxide reductase, that protects cells from damage caused by oxygen-free radicals. These radicals are rogue molecules produced by breathing that are thought to crash into cells, destroying their genetic material. "This enzyme could scavenge free radicals that are theorized to be one of the causes of aging. And that's what we observed, says Jakob Moskovitz, a researcher at the Heart, Lung and Blood Institute. Mr. Moskovitz says the enzyme also repairs damage to cells caused by oxygen-free radicals.

He and his colleagues saw the beneficial effects of the enzyme when researchers bred mice that were missing the gene, so-called "knock-out mice." The knock-out mice began showing nerve damage at six months of age, and their life span, on average, was 10 percent shorter than normal rodents'. The results of the study are published in the Proceedings of the National Academy of Sciences.

Researcher Moskovitz says the same gene identified in the paper exists in humans. "Now maybe people who live shorter lives ... may have some problems with the gene," he says. "Now, if the theory is that, if you over-express this gene, making more copies of it by intervention, you may extend the life span of normal human beings."

But this is just a theory that would have to be demonstrated in the laboratory.

Stephen Spindler, a biochemistry at the University of California, says the study by federal researchers shows a fully functioning anti-oxidant system is essential for normal life span and the complete health of animals. "I think the limitation of the study is that it's not hard to create transgenic animals that have knocked out essential functions that shorten their life span," he says. "So the study doesn't prove the [oxygen] free radical theory of aging."

Mr. Spindler's own work has looked at the beneficial effects of a low-calorie diet on aging. He found that putting mice on a very low calorie diet for as little as one month reversed many of the changes associated with growing old.

It's thought that eating less reduces the production of damaging free radicals. A restricted diet is the treatment that's been shown to extend the life span of mammals.

Franklin Williams is scientific director for the American Federation for Aging Research. He says the latest research is useful in the study of aging. "And it gives some more evidence on the value of anti-oxidants or reducing the damage that oxidation may cause in our bodies in relation to life span," he says.

Dr. Williams notes the purpose of anti-aging research is not only to increase life span, but improve the quality of life of those who are living longer.

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