Biotechnology

Molecular Fountain of Youth Discovered

Jan 31, 2013 12:51 PM ET // by Nic Halverson

Recapturing youth my require scientists to harness a protein called SIRT3 that could prevent diseases associated with aging.

Felipe Rodriguez Fernandez/Getty Images

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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, they’re 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. That’s right, they’re not just offering a sip from the fountain, they’re 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. It’s 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. It’s really the next big step.”
Chen cited molecular biologist Cynthia Kenyon’s 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 can’t 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.
“We’re particularly interested in SIRT3,” Chen said, “because we found that it’s 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. “It’s certainly not acting as a transcription factor, it’s 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 weren’t seeing any differences between the wild mice and the SIRT3 knockout mice.”