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.
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.
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.
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.
No comments:
Post a Comment