Is the prospect of extending the human lifespan a matter of turning up the dial on a single gene? Researchers at the University of California in Los Angeles show that it might be.

The scientists, headed up by associate professor David Walker, tweeked the amount of a protein called AMPK in the intestines of fruit flies by turning on the gene that encodes the protein. The result was that the flies with more AMPK in their intestines lived longer.

“We have shown that when we activate the gene in the intestine or the nervous system, we see the aging process is slowed beyond the organ system in which the gene is activated,” Walker said in a statement.

Humans also possess the gene that encodes for AMPK, but it normally operates at a low level. Walker said that identifying a target gene for extending longevity in a relatively accessible tissue or organ is paramount.

“Instead of studying the diseases of aging — Parkinson’s disease, Alzheimer’s disease, cancer, stroke, cardiovascular disease, diabetes — one by one, we believe it may be possible to intervene in the aging process and delay the onset of many of these diseases,” said Walker, a member of UCLA’s Molecular Biology Institute. “We are not there yet, and it could, of course, take many years, but that is our goal and we think it is realistic.

The protein AMPK has been previously shown to activate a cellular process called “autophagy,” which is a means for cells to dispose of cellular and molecular “garbage.” Doctoral student and lead author Matthew Ulgherait set out to determine whether activation of AMPK in the flies increased the rate at which autophagy proceeded. It did, even in distant tissues such as the brain.

“Matt moved beyond correlation and established causality,” said Walker. “He showed that the activation of autophagy was both necessary to see the anti-aging effects and sufficient; that he could bypass AMPK and directly target autophagy.”

According to Walker, the drug metformin used to treat Type 2 diabetes activates AMPK.