Scientists discover ways to slow down the aging of mice
- April 07, 2015
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Biologists have described a method by which they say they can double the lifespan of prematurely aging mice.
Whether the findings would apply to humans, and even normal aging, is unclear, but there are some promising signs, they add. The results suggest that folic acid, already prescribed for certain symptoms of aging, may have a role.
In 2009 researchers from the Spanish National Cancer Research Centre under the leadership of Óscar Fernández-Capetillo described how mice with low levels a protein called ATR, needed for DNA repair, age prematurely. In the new paper, published in the journal Genes & Development, they describe how they fixed this: introducing a mutation that can boost the body's production of DNA components called nucleotides, or dNTPs.
The authors built on previous research with yeast, which had strains suffering from ATR mutations, like the mice. “Although yeast does not age as such,” the mutation hurts both organisms, wrote the researchers.
They created mice that-along with the original mutation causing premature aging-also had multiple copies of Rrm2, the key gene for making nucleotides. The result was the boosted lifespan, from an average of 24 weeks to 50 weeks, the investigators said. The ATR-mutant mice were based on a human disease called Seckel syndrome, originally known as “bird-headed dwarfism.” The newly introduced mutation not only improved the aging but other symptoms, the researchers said.
Every living thing has certain fragile areas in its genome. These tend to break, and have been tied to diseases including cancer. The authors argue that mice with extra copies of Rrm2 suffered less of these breaks.
Whether the results are relevant to normal, rather than premature aging remains to be seen, the scientists said. But they note that standard medical practice includes prescribing folic acid (or vitamin B12) supplements to the elderly to delay or lessen the degenerative symptoms associated with advanced age. Folic acid is, among other things, a precursor molecule in making DNA components like those produced by Rrm2.
“The question we are asking ourselves now” is whether whether a similar change “could also lengthen life expectancy in normal animals without premature ageing,” said Fernández-Capetillo. Co-author Andrés López-Contreras plans to continue the work as head of a laboratory at the University of Copenhagen.