Molecular Fountain of Youth Discovered
Jan 31, 2013 12:51 PM ET // by Nic Halverson
Recapturing youth may require scientists to harness a protein called SIRT3 that could prevent diseases
associated with aging. Four thousands of years, our thirst for the legendary Fountain of Youth has been nearly
as strong as our propensity for perpetuating the myth.
However, over the last 20 years, the fertile headwaters of molecular biology have been pumping out anything
but folklore. Not only have these waters yielded a precipitous stretch in understanding the aging process,
theyre potentially guiding us closer to the source of everlasting youth.
From this flow now comes word that biologists from the University of California, Berkeley have tapped an
influential longevity gene that can reverse cell degeneration associated with aging. Thats right, theyre not just
offering a sip from the fountain, theyre turning back the clock at the molecular level.
The new study, published in Cell Reports, represents a major discovery and offers new hope for development of
targeted treatments for a long list of age-related degenerative diseases, such as heart disease, Alzheimer's and
arthritis, just to name a few.
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The biologists, lead by UC Berkeley assistant professor of nutritional science and toxicology Danica Chen,
focused their attention on one protein in particular: SIRT3. Its one in a class of proteins called surtuins, long
known to regulate aging.
Biologists found that SIRT3 plays a significant role in helping aged blood stem cells cope with the oxidative
stress of the aging process. When the blood stem cells of aged mice were infused with SIRT3, it regenerated
new blood cells, providing evidence of a reversal in the age-related degeneration of the cells function.
This is really the first demonstration that sirtuins may be able to actually reverse aging-associated
degeneration, Chen told Discovery News.
We known aging can be regulated so we may be able to manipulate the molecular pathways and slow down the
process, she added. But there's never been a demonstration where we could reverse age. Its really the next
big step.
Chen cited molecular biologist Cynthia Kenyons pioneering work in the early 1990s as perhaps the biggest
breakthrough in understanding that aging is not a random, uncontrolled process, but rather a highly regulated
development. In 1993, Kenyon published a study in Nature that showed a single gene mutation in a tiny worm
(C. elegans) could double its lifespan, opening up the floodgates of intensive studies on age manipulation.
We know there are a lot of techniques out there, said Chen. For example, you can use transgenic mouse
models to upregulate sirtuins to increase the quality of a cell but those only address the question of whether
you can slow aging. But you cant really address the question of whether you could reverse aging.
Unless, of course, you find the right key, which Chen and colleagues may have found in SIRT3.
Were particularly interested in SIRT3, Chen said, because we found that its highly enriched in
hematopoietic stem cells. These are blood stem cells, highly regarded for their ability to completely
reconstitute the blood system, the underlying capability of a successful bone marrow transplant.
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Also of interest is the location of where SIRT3 is found “ in the mitochondria, the cell compartment that helps
control growth and death.
What I liked so much about our study is that SIRT3 is mitochondrial, said study co-author Dr. Katharine
Brown. Its certainly not acting as a transcription factor, its effecting metabolism and other aspects of cell
signaling, which is clearly very important in aging. Brown conducted the research as a Ph.D. student in Chen's
lab.
To gauge the effects of aging, researchers observed the blood system of young mice that had the SIRT3 gene
disabled. At first, the absence of SIRT3 made no difference on the young mice.
This study definitely took a few years, said Brown. It was kind of frustrating at the beginning because we
werent seeing any differences between the wild mice and the SIRT3 knockout mice.
