Aging in old mice was reversed by researchers by injecting them with a longevity gene and rejuvenating their stem cells' regenerative potential.
The study by University of California-Berkeley biologists represents a major advance in understanding the molecular mechanisms behind aging, paving the way for the development of targeted treatments for age-related degenerative diseases.
The found that SIRT3, one among a class of proteins known as sirtuins, plays an important role in helping aged blood stem cells cope with stress, the journal Cell reports.
When they infused the blood stem cells of old mice with SIRT3, the treatment boosted the formation of new blood cells, evidence of a reversal in the age-related decline in the old stem cells' function, according to a California statement.
"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," said study principal investigator Danica Chen, assistant professor of nutritional science and toxicology. "This opens the door to potential treatment for age-related degenerative diseases."
Instead of an uncontrolled, random process, aging is now considered as highly regulated as development, opening it up to possible manipulation. "Studies have already shown that even a single gene mutation can lead to lifespan extension," said Chen.
The researchers first observed the blood system of mice that had the gene for SIRT3 disabled. Surprisingly, among young mice, the absence of SIRT3 made no difference. It was only when time crept up on the mice that things changed.
By the ripe old age of two, the SIRT3-deficient mice had significantly fewer blood stem cells and decreased ability to regenerate new blood cells compared with regular mice of the same age.