Scientists delay aging process by remote control

The global anti-aging market is projected to be worth USD 191.7 billion by 2019. This shows that people are willing to pay anything to remain young – no wrinkles, greys, arthritis, rheumatism etc. It is no wonder then that scientists have been working to find a way of stopping or at least delaying the aging process.

Experimenting with fruit flies (Drosophila melanogaster), the scientists activated a gene called AMPK (‘ Adenosine Monophosphate-activated Protein Kinase), a key energy sensor in cells which gets activated when cellular energy levels are low.Late last year, scientists at the University of California, Los Angeles (UCLA) recorded a breakthrough as they identified a gene that can slow the aging process in the entire body when activated remotely in key organ systems such as the liver, brain and skeletal muscle.

By increasing the amount of AMPK in the intestines of fruit flies, they discovered their lifespans increased by about 30 per cent (from the typical six weeks to eight weeks) and the flies stayed healthier for a longer period as well. According to David Walker, Associate Professor of Integrative Biology and Physiology at UCLA and senior author of the research, the research reported in the open-source journal, Cell Reports, could have important implications for delaying aging and disease in humans.

Said Walker: “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.”

He noted that the findings are important because extending the healthy life of humans would presumably require protecting many of the body’s organ systems from the ravages of aging—but delivering anti-aging treatments to the brain or other key organs could prove technically difficult. The study suggests that activating AMPK in a more accessible organ such as the intestine, for example, could ultimately slow the aging process throughout the entire body, including the brain.

“Humans have AMPK, but it is usually not activated at a high level. Instead of studying the diseases of aging—Parkinson’s, Alzheimer’s, cancer, stroke, cardiovascular disease and 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,” he said.

“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.” The fruit fly is a good model for studying aging in humans because scientists have identified all of the fruit fly’s genes and know how to switch individual genes on and off. The biologists studied about 100,000 fruit flies in the course of the study.

Lead author, Matthew Ulgherait, who conducted the research as a doctoral student, focused on a cellular process called autophagy, which enables cells to degrade and discard old, damaged cellular components. By getting rid of that “cellular garbage” before it damages cells, autophagy protects against aging, and AMPK has been shown previously to activate this process. Ulgherait studied whether activating AMPK in the flies led to autophagy occurring at a greater rate than usual.

“A really interesting finding was when Matt activated AMPK in the nervous system, he saw evidence of increased levels of autophagy in not only the brain, but also in the intestine,” said Walker. And also, activating AMPK in the intestine produced increased levels of autophagy in the brain—and perhaps elsewhere, too.”

Walker noted that many neurodegenerative diseases, including Alzheimer’s and Parkinson’s, are associated with the accumulation of protein aggregates, a type of cellular garbage, in the brain. “Matt moved beyond correlation and established causality,” he 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.”

Walker said that AMPK is thought to be a key target of metformin, a drug used to treat Type 2 diabetes, and that metformin activates AMPK. The research, funded by National Institutes of Health’s National Institute on Aging and other agencies, has as co-authors Anil Rana, a post-doctoral scholar in Walker’s lab; Michael Rera, a former UCLA post-doctoral scholar in Walker’s lab; and Jacqueline Graniel, who participated in the research as a UCLA undergraduate.