THURSDAY, Jan. 31 (HealthDay News) -- A discovery about the aging process in mice might one day help efforts to develop treatments for age-related diseases in humans, researchers report.
The biologists say they turned back the "molecular clock" in old mice by placing a "longevity" gene into their blood stem cells.
The gene, called SIRT3, belongs to a class of proteins called sirtuins, which help aged blood stem cells handle stress. Placing SIRT3 into the blood stem cells of old mice increased the formation of new blood cells, the investigators found. This, according to the researchers, is evidence of a reversal in the age-related decline in the old stem cells' function.
"We already know that sirtuins regulate aging, but our study is really the first one demonstrating that sirtuins can reverse aging-associated degeneration, and I think that's very exciting," study principal investigator Danica Chen, an assistant professor of nutritional science and toxicology at the University of California, Berkeley, said in a university news release.
The finding "opens the door to potential treatments for age-related degenerative diseases," Chen said.
The study was published online Jan. 31 in the journal Cell Reports.
Research over the past 10 to 20 years has led to breakthroughs in the understanding of aging, Chen said. Whereas aging had been previously looked upon as a random and uncontrolled process, it is now believed to be highly regulated and possibly even open to manipulation, she noted.
"Studies have already shown that even a single gene mutation can lead to lifespan extension," Chen said. "The question is whether we can understand the process well enough so that we can actually develop a molecular fountain of youth. Can we actually reverse aging? This is something we're hoping to understand and accomplish."
Experts note, however, that results from animal research are not always able to be replicated in humans.
The U.S. National Institute on Aging offers healthy aging tips.
-- Robert Preidt
SOURCE: University of California, Berkeley, news release, Jan. 31, 2013
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