Researchers from the University of California-Los Angeles say they have discovered a gene that, when activated in key organs including the intestines and brain, could slow the aging process of the whole body.

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Researchers found that activating a gene called AMPK in the intestines of fruit flies increased autophagy - a process that protects against aging - in both the intestines and the brain, and vice versa.
Image credit: Matthew Ulgherait/UCLA

The research team - led by Matthew Ulgherait, an associate professor in the Departments of Integrative Biology and Physiology and Biological Chemistry at the University of California-Los Angeles (UCLA) - says their findings may offer a strategy for delaying aging and disease in the human body.

For their study, recently published in the journal Cell Reports, Ulgherait and his team focused on autophagy - a process in which cells break down and dispose of its old or broken parts before the cells are damaged beyond repair.

This process protects against aging, the team says, noting that previous research has indicated that a gene called AMPK activates autophagy.

As such, the researchers wanted to see how activating the AMPK gene in Drosophila melanogaster, more commonly known as the fruit fly, influenced the aging process.

The fruit fly is an ideal model in which to study human aging, they explain, because scientists have identified all of its genes and know how to activate and deactivate each of them.

Activating AMPK gene 'increased lifespan of fruit flies by 30%'

The researchers were surprised to find that when they activated the AMPK gene in the nervous system of the flies, autophagy was increased in both the brain and intestine. And when activating the gene in the intestine, autophagy was increased in the brain, intestine and other areas of the body.

Activating the AMPK gene in the intestine increased the lifespan of the fruit flies by around 30% - from the usual 6 weeks to 8 weeks - according to the team, and it also increased the length of time the flies remained healthy.

"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," says senior study author David Walker of the Department of Integrative Biology and Physiology and the Molecular Biology Institute at UCLA.

When it comes to protecting humans against the aging process, it goes beyond the skin. Walker notes that human organs also need protecting from age-related disease, but he says that delivering anti-aging treatments to the brain or other major organs is challenging.

He says that these findings, however, suggest that the aging process of the entire body - including the brain - may be delayed simply by activating the AMPK gene in an organ that is more accessible, such as the intestine.

Speaking of what these findings could hold for the future, Walker says:

"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.

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 ultimate aim of our research is to promote healthy aging in people."

This is not the first time Walker and colleagues have identified a gene associated with aging. Last year, Medical News Today reported on a study from the team in which they found that a gene called parkin - thought to contribute to a form of Parkinson's disease - could extend the lifespan of fruit flies by 25%.

Although he does not delve into detail, Walker mentions that metformin - a drug approved for the treatment of type 2 diabetes - is known to activate the AMPK gene.

Medical News Today recently reported on a study by researchers from Cardiff University in the UK, which found metformin increased lifespan in humans. Another study earlier this year by Belgian researchers found metformin produced similar results in the roundworm C. elegans.