In an experiment on fruit flies, UCLA biologists activated just one gene, AMPK, which extended their lifespan by nearly a third, by helping them to get rid of “cellular garbage” causing old age diseases such as Parkinson’s. Humans have the same gene.
“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 author David Walker, an associate professor of integrative biology and physiology at UCLA, whose paper was published last week in the scientific journal Cell Reports.
“We are not there yet, and it could, of course, take many years, but that is our goal and we think it is realistic.”
UCLA’s laboratory conducted the study on 100,000 fruit flies, used because they have been genetically mapped, and scientists can easily mutate just one gene within a population, limiting variables, and ensuring a perfectly controlled experiment.
Those flies with the gene activated in their intestines lived just over eight weeks, instead of the usual six, and, almost as crucially, remained healthier for longer into their lifespans. Projected onto the current US life expectancy of 78, this would correspond to an average lifetime of 101 years.
The impressive results were achieved by activating a process called autophagy, which is stimulated by AMPK.
Autophagy which translates from Greek as ‘eating oneself’ allows cells to isolate and discard old, dysfunctional fragments, known as cellular garbage, which can damage healthy cells. Many of the old-age diseases are widely thought to result from decreased rates of autophagy, which eventually build up millions of unhealthy cells in the body.
While humans have the AMPK gene, in most people, it is ‘turned off’.
Researchers also found that switching on the gene in one part of the body results in its activation elsewhere.
“A really interesting finding was when [lead author] Matthew Ulgherait activated AMPK in the nervous system, he saw evidence of increased levels of autophagy in not only the brain, but also in the intestine. And vice versa: Activating AMPK in the intestine produced increased levels of autophagy in the brain and perhaps elsewhere too,” Walker said.
This means that in the future, doctors could perform treatments in easier to reach areas, such as the stomach, even though the main benefits of the therapy could be in harder-to-access ones, like the brain.
The wider conclusions drawn by the team are not just about the single gene AMPK, but demonstrate the key role of autophagy in longevity.
“Matt moved beyond correlation and established causality,” Walker said. “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.”
Intriguingly, while the benefits of genetic AMPK treatment appear to be years away, there is already a drug on the market that stimulates existing AMPK genes, which are activated when cells reach a low energy level, as a sort of repair mechanism.
Metformin was synthesized as long ago as 1922, and has been widely used to fight diabetes since the late 1950s, and can now be bought cheaply as a generic. Despite considerable side effects, in recent years it has been touted in multiple studies as decreasing the incidence of cancer and heart disease, and is already used by some as an anti-aging drug, though it cannot be prescribed as such. This appears to dovetail with UCLA’s research on AMPK, which was acknowledged by Walker, who stopped short of advising healthy people to take metformin.
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