BIOLOGISTS DELAY THE AGING PROCESS BY REMOTE CONTROL
U CLA biologists have
identified a gene that can slow the aging process throughout the entire body
when activated remotely in key organ systems
Working with fruit
flies, the life scientists activated a gene called AMPK that is a key energy
sensor in cells; it gets activated when cellular energy levels are low.
Increasing the amount
of AMPK in fruit flies' intestines increased their lifespans by about 30
percent -- to roughly eight weeks from the typical six -- and the flies stayed
healthier longer as well.
The research,
published Sept. 4 in the open-source journal Cell Reports, could
have important implications for delaying aging and disease in humans, said
David Walker, an associate professor of integrative biology and physiology at
UCLA and senior author of the research.
"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.
Walker said 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, Walker said.
"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 ultimate aim
of our research is to promote healthy aging in people."
The fruit fly, Drosophila
melanogaster, 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 approximately 100,000 of
them over the course of the study.
Lead author Matthew
Ulgherait, who conducted the research in Walker's laboratory 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, a faculty member in the UCLA College.
"And vice versa: Activating AMPK in the intestine produced increased
levels of autophagy in the brain -- and perhaps elsewhere, too."
Many neurodegenerative
diseases, including both Alzheimer's and Parkinson's, are associated with the
accumulation of protein aggregates, a type of cellular garbage, in the brain,
Walker noted.
"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 was
funded by the National Institutes of Health's National Institute on Aging
(grants R01 AG037514 and R01 AG040288). Ulgherait received funding support from
a Ruth L. Kirschstein National Research Service Award (GM07185) and Eureka and
Hyde fellowships from the UCLA department of integrative biology and
physiology.
Co-authors of the
research were Anil Rana, a postdoctoral scholar in Walker's lab; Michael Rera,
a former UCLA postdoctoral scholar in Walker's lab; and Jacqueline Graniel, who
participated in the research as a UCLA undergraduate.
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