Key To Aging: Mitochondrial DNA

Gray hair — or no hair — wrinkles and creaky joints are obvious reminders that you're not getting any younger.

Scientists in Sweden say aging begins in a more fundamental way — in the accumulation of tiny changes to a mysterious genetic component in cells called mitochondrial DNA.

Researchers describe the study as the first experimental evidence of this theory — at least in laboratory mice. They believe the finding could explain how humans age and how the body's systems begin to misfire, although more tests must bear out them out. The mouse results appear in the current issue of the journal Nature.

"It seems to be a universal phenomenon in mammals that you have this damage to mitochondrial DNA as you get older," said the study's senior author, Nils-Goran Larsson at the Karolinska Institute in Stockholm.

"But I and many others thought this was just a secondary phenomenon," Larsson said. "I think the importance of our paper is that we actually show these mutations can indeed cause several changes associated with aging."

Other scientists say the Swedish experiments clearly show that a high rate of mutation in mitochondrial DNA has an effect on aging.

"But that does not mean all aging is caused by mutations in mitochondrial DNA," said David Finkelstein of the U.S. National Institute on Aging, part of the National Institutes of Health.

In the experiments, the Swedish team used mice bred with a defective version of an enzyme responsible for maintaining mitochondrial DNA.

Mitochondria are tiny biochemical power plants in cells that convert food into energy. Mitochondria contain strands of their own DNA that are separate from the cell nucleus where the body's genes reside.

The deterioration in the experimental mice started at 25 weeks — young adulthood in normal mice. They prematurely experienced a range of familiar age-related complaints, including baldness, osteoporosis, anemia, curvature of the spine and reduced fertility. The lifespan of the experimental mice was markedly reduced, with the median age of death at 48 weeks. The oldest of the experimental mice died before 61 weeks.

In normal mice, early aging signs appear at about 40 weeks. Emaciation and other signs of old age accumulate by 1.5 years, and lab mice typically live a little over 2 years.

In an accompanying commentary in Nature, George Martin and Lawrence Loeb of the University of Washington said the results are also consistent with the theory that so-called "free radicals" play a role in aging.

Free radicals typically are oxygen molecules that lack an electron, often setting up a corrosive chain reaction that can damage other cells.

Regardless of how aging begins, researchers said the steps to extend a healthy, youthful life are familiar and simple.

"Watch what you eat, exercise, don't smoke, keep your mind active," Finkelstein said, "and you're more likely to live longer."