Researchers at the California Institute of Technology have discovered a key genetic mutation common in humans that could help significantly extend people's lives, a finding some Penn State professors are wary of accepting.

The study, published in the latest edition of the journal Proceedings of the National Academy of Sciences, examined the mitochondrial DNA of 52 Italian people who were age 100 or older. Scientists found that the site where these individuals' mitochondrial DNA copied itself was slightly shifted. Though a small change, this could speed up replication and how fast damaged cells can fix themselves.

The complexity of mitochondria, along with the intricate processes of aging, are what lead some Penn State professors to be wary about the results of the study.

"The mitochondria is a tricky little beast," said Mitch Price, instructor of biology. "This seems like an oversimplification of things."

However, Giuseppe Attardi, Caltech professor of molecular biology, and an author of the study, said the mutation has a clear impact on the body.

"It is possible that this mutation makes the mitochondria less damaged" than they would be in a person lacking this mutation, Attardi said. "This mutation encourages survival."

Mitochondria are viewed as the "powerhouses" of the cell--they are responsible for energy production and programmed cell death. Mitochondria also work with antioxidants to combat the harmful effects of atoms called free radicals. Free radicals have been shown to cause aging-related diseases such as Alzheimer's and Parkinson's, as well as conditions such as cataracts. Because aging is the accumulation of harmful mutations, cellular damage, and other deterioration that occurs over the lifetime, mitochondria work to fix these problems as much as possible.

"On the surface, this study suggests this mutation ramps up the ability to protect us from free radicals, and/or ramps down the ability of programmed cell death," Price said.

Other recent longevity studies have suggested that the cell death response brought about by mitochondria actually contributes to aging and some of the neurological disorders, such as Alzheimer's disease, that accompany it.

Robert Mitchell, professor of biology, advised using caution when reading any published study.

"Aging is the result of hundreds of thousands of different things; no one thing, no one gene. It's like behavior, or being smart. No one thing makes you smart. So that this discovery would be the only thing responsible would be unlikely."

Attardi disagreed.

"What this mutation does is encourage survival," he says. "This mutation cannot possibly have a negative effect."

He does concede that a great deal of further study needs to be done before any practical application can come of this discovery. Any applications would most likely come about in the form of drugs or treatment therapy to extend the duration of a person's life.

The maximum lifespan for any human being is about 120 years, Mitchell said, and has not changed throughout time. What scientists have done over the years is increase life expectancy, which has increased from 50 years to about 80 years within the last century.

At some point in the lifespan, the real question becomes: "Is aging a relevant therapeutic target? I don't know if it is," Price said. "But in order to make it better, we still have a long way to go, but this is certainly a spoke in our wheel of understanding."