Sunday, April 5, 2015

Doubling Lifespan of Mice


In 2009, it was shown by the Spanish National Cancer Research Center under Óscar Fernández-Capetillo that mice age faster with low levels of ATR protein, an essential protein for the repair of damaged DNA, Stopping the premature ageing of these mice and doubling their life span has been achieved by introducing a mutation capable of increasing the body's capacity to produce nucleotides available in the cell.

This was originally tested in yeast, Saccharomyces cerevisiae, where it proved to be true and has since been tested on mice. The mice were given two genetic alterations with the first being the original ATR gene mutation that led to premature aging and the second which was the animals had multiple copies of Rrm2, the key gene for nucleotide synthesis. The results showed the aging process to be significantly slowed in these mice, taking their life span from 24 weeks to 50 weeks.

Every genome has weak or fragile sections which break spontaneously. These fragile sections have been shown to be involved in human diseases like cancer. The research paper showed that those mice with additional copies of Rrm2 suffered less DNA breaks in these fragile areas. "The question we are asking ourselves now is whether an increase in the capacity to produce nucleotides could also lengthen life expectancy in normal animals without premature ageing," says Fernández-Capetillo.

I found this article very interesting due to the research of prolonging and increasing the life span of animals. Although it is not said in the article I think it goes without saying that the obvious implications of a study like this is to eventually see if causing these same mutations in humans could lead to longer and healthier life spans.



2 comments:

  1. I personally think that increasing the lifespan of things is dangerous. Organisms have short or long lifespans, respectively, for a reason and elongating them could pose problems. However, if this process could lead to longer lifespans without complications, it may be interesting to carry on with. But the longer something is alive, the more susceptible it is to sickness and disease so scientists must keep that in mind. It seems as though they have it under control but I'm curious to see how other organisms react to the procedure.

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  2. I think that this research could go a long way in improving longevity, but more importantly quality of life. Like the article says, a lot of human diseases, including forms of cancer, derive from damage to nucleoides. If this artificial mutation can prevent damage to genes, it could potentially prevent serious diseases within humanity. Then again, nature is perpetually adapting, so altering our genes one way could result in harmful alterations down the line - either within the lifespan or in successive generations. While this research shows promise, a lot more work has to go into it, and I wouldn't trust this as stable until later generations are produced after the parental generations being exposed to this type of treatment.

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