LOS ANGELES (AP) — Researchers extended the lifespan of the fruit fly by giving it an extra gene that boosted its ability to remove wastes from its cells — a potentially promising approach in the effort to stem the ravages of aging and disease in humans.
The gene was inserted in the insects' motor neurons, which are nerve cells that control movement. It extended the fruit flies' 80-day lifespans by as much as 40 percent.
Providing a fruit fly with another month on Earth may not sound like much. And whether it will work in humans or even mice remains to be seen. But the implications are tremendous, the researchers and outside experts said.
"It's incredibly striking to me that you can extend the lifespan" via a single gene, said Tom Johnson, a professor at the Institute for Behavioral Genetics at the University of Colorado at Boulder who was not connected to the research. "It really speaks very optimistically for our ability to directly intervene into the aging process in other higher animals, including humans."
The study was published in the June issue of the journal Nature Genetics. It was led by Gabrielle Boulianne, a neurobiologist at the Hospital for Sick Children and a professor of molecular and medical genetics at the University of Toronto.
Ms. Boulianne said the findings mark the first time researchers have shown a single gene in a single type of cell can affect longevity.
"We were really surprised," she said. "We never expected manipulating a single gene like this would have such profound effects on lifespan."
Humans, of course, are far more complicated creatures than fruit flies. But Ms. Boulianne said that the findings suggest that the aging process in humans might be much simpler than scientists ever suspected.
The work stems from the central fact that oxygen is damaging to the body. While oxygen provides living things with their energy, its byproducts produce cell damage and death. The process can be thought of as cellular rusting.
All cells in insects and animals naturally produce an enzyme called superoxide dismutase that converts wastes into harmless substances.
Some cases of Lou Gehrig's disease and Alzheimer's are known to be caused by mutations in the gene that tells cells to make this enzyme. The resulting shortage of enzyme allows wastes to build up and destroy motor neurons.
So Ms. Boulianne began wondering what would happen if she enhanced motor neurons' ability to eliminate the wastes.
She bred fruit flies with copies of the human SOD1 gene, which instructed the insects' cells to make extra enzyme. When the nerve cells made more enzyme, the flies lived longer.
The findings suggest that the nervous system is a primary target of the aging process, Ms. Boulianne said.
"It's really cool stuff," said Caleb E. Finch, director of neurogerontology at the University of Southern California in Los Angeles.
"This particular study now shows that targeted protection of nerve cells may have an advantage not only to human diseases of aging, such as Alzheimer's, but may have more general roles in aging and lifespan limitations throughout the animal kingdom."
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