Slashdot is powered by your submissions, so send in your scoop


Forgot your password?
Medicine Science

Changing a Single Gene Allows Mice To Live 20 Percent Longer 79

An anonymous reader writes "A research team at the National Heart, Lung, and Blood Institute has been experimenting with changing mouse genes and seeing how it impacts their life. In a surprising discovery, when targeting just one gene change it was found they could extend the life of a mouse by 20 percent. The gene the researchers focused on is called mTOR and is associated with metabolism. By lowering its expression (to about 25 percent of what is normal) in a batch of mice they did indeed live longer (abstract). They also displayed better memory, balance, muscle strength, and posture as they aged. However, the health of their bones deteriorated more quickly and their immune system was weakened, suggesting that extra time alive wouldn’t really be worth it in terms of overall health. Lead researcher Toren Finkel said, 'While the high extension in lifespan is noteworthy, this study reinforces an important facet of aging; it is not uniform. Rather, similar to circadian rhythms, an animal might have several organ-specific aging clocks that generally work together to govern the aging of the whole organism.'"
This discussion has been archived. No new comments can be posted.

Changing a Single Gene Allows Mice To Live 20 Percent Longer

Comments Filter:
  • by Anonymous Coward

    at least for now...

  • Blatant conjecture (Score:2, Insightful)

    by Anonymous Coward

    "an animal might have several organ-specific aging clocks that generally work together to govern the aging of the whole organism."

    I see nothing to support the idea of a "clock." If aging were regulated by a clock-like process, then it would seem reasonable that you could just stop the clock. "Solving" the aging problem would be just a matter of eliminating the regulation circuitry.

    Anyone who does engineering should realize that's a naive assumption. Since there are no animals that live forever, you have to

    • by ElectricTurtle ( 1171201 ) on Saturday August 31, 2013 @08:36PM (#44727539)
      Actually you are wrong, there is at least one organism that can live forever: the turritopsis nutricula []
    • by houstonbofh ( 602064 ) on Saturday August 31, 2013 @08:37PM (#44727551)

      Since there are no animals that live forever, you have to assume that extending life is a totally new feature... not a bugfix.

      Really? []

      Hey! Cracked is at least as reliable as CNN, fox, or MSNBC, and lately it is more unbiased.

    • Telomeres function as a kind of clock:

      The telomere-shortening mechanism normally limits cells to a fixed number of divisions, and animal studies suggest that this is responsible for aging on the cellular level and sets a limit on lifespans. Telomeres protect a cell's chromosomes from fusing with each other or rearranging—abnormalities that can lead to cancer—and so cells are destroyed when their telomeres are consumed. Most cancers are the result of "immortal" cells that have ways of evading thi

    • If aging were regulated by a clock-like process, then it would seem reasonable that you could just stop the clock

      You can. It's called killing them.

  • Talk about a gray moment here. For some reason, I thought the headline said Makes Mice 20% Cooler.

    • That'd be a hard decision if I had to pick if I was 20% cooler or live 20% longer. I guess it is the same decision for people who think cigarettes are cool(hint: they're not).
    • by slick7 ( 1703596 )

      Talk about a gray moment here. For some reason, I thought the headline said Makes Mice 20% Cooler.

      Not really a grey moment, only the rich and politically influential mice are 20% cooler and live 20% longer, the regular mice, not so much.

  • by timeOday ( 582209 ) on Saturday August 31, 2013 @08:56PM (#44727633)
    ...burns twice as long? Having a lower metabolism sounds like it would just be life in slow motion. Granted the increase in muscle strength seems contrary to this and is surprising. But still, a lower metabolism must mean less energy and vigor.
    • "must" is a strong word. Never use it. For instance: Lower metabolism but higher efficiency. You done DERPed, son.
    • Changing the expression of mTOR isn't impacting all of your metabolism, that's not actually what's happening here. It's just changing a single aspect of metabolism.

    • You know what's a hoot. I have (and had) some hippy aunts and uncles that subscribed to these hippie and back to nature magazines in the 70s, and there were these heroes of diet who were pushing low calorie diet for longevity. One very famous one even claimed he was going to reach 150 eating carrots, sprouts and such shit. Anyway, the punchline is that all of these super diet Methuselahs have one thing in common, they are all very dead. I don't recall any of them making it out of their 70s in fact.

      On th

    • by Meski ( 774546 )
      That's a Batty comment you just made. (and he didn't like it much, if his response was anything to go by)
  • by Anonymous Coward

    How do we measure mouse posture? They stand up straighter?

  • As engineer, I have over 30 years of career been confronted with some problems, items to adjust and calibrate, etc.
    And I can vouch for the fact that in almost all cases, there was a trade-off. One parameter increasing, another would decline; e.g. MTBF. Or efficiency. Therefore, how can fiddling arbitrarily with parameters on a system constitute research?
    News at 11.
    Wake me up when a longer life is possible without side-effects.

    • by Anonymous Coward
      Biology is several orders of orders of magnitude more complex than the toy-like systems you dealt with in engineering. One single cell is so mind bogglingly complex that you could spend your life studying one cell, never mind how it grew from a stem cell and how it relates to the billions of other cells in the body (a system of systems on a scale to dwarf the entire Internet, in every body.)

      You learned a few equations, learned about crystal aging and a few systems to make a handful of atoms vibrate in a sp

      • by udippel ( 562132 )

        Why don't you help with anti-aging efforts?

        This is actually a very good question. Thanks for asking it.
        It is because I don't see any progress if it could be achieved. Imagine an ever increasing amount of biomass being used up for an ever increasing number of human beings. At times, old age and death is a great contributor to human progress. Stalin and Mugabe spring into mind. If we were here for eternity all my stereotypes, my convictions, my undue biases would be there forever.
        However, me dying opens space for someone to pick up from me, and maybe

  • by Anonymous Coward

    After changing one more mouse gene, a crashing sound is heard from the lab.
    The metal mouse cage is torn apart and there's a hole in the brick wall.
    People outside the building are yelling... look up in the sky, it's a bird, a plane, superman.. no that's not superman!..
    it's "Mighty Mouse"!
    "Here I come to save the day!"

  • by roninchurchill ( 2991659 ) on Saturday August 31, 2013 @09:55PM (#44727913)

    The research may be new, but it encounters the same old problem: increasing the lifespan of a mouse by 25% (hint: it's measured in months) is much different than increasing human lifespan. The last "anti-aging miracle" I read about, lowering IGF-1 levels, provided just as much misguided hope. Mice with low levels of IGF-1 lived longer--surely the same must be true for humans too, right? Not quite... low levels of IGF-1 are associated with higher risk of ischemic heart disease, and may also be associated with greater risk for sarcopenia.

    Do more people die from reaching the natural limit to their life, or from heart disease and complications due to fractures? Until a research team can demonstrate that altering these pathways provides tangible human benefit (without a hidden consequence), we're just learning how to increase our favorite pet rodent's life.


    Laughlin GA, Barrett-Connor E, Criqui MH, Kritz-Silverstein D. The prospective association of serum insulin-like growth factor I (IGF-I) and IGF-binding protein-1 levels with all cause and cardiovascular disease mortality in older adults: the Rancho Bernardo Study. J Clin Endocrinol Metab. January 2004;89:114-20.

    Giovannini S, Marzetti E, Borst SE, Leeuwenburgh C. Modulation of GH/IGF-1 axis: potential strategies to counteract sarcopenia in older adults. Mech Ageing Dev. October 2008;129:593-601. doi: 10.1016/j.mad.2008.08.001.

  • Or a repressive protein that blocks the operating cells?

  • Give me quality please.
  • mTOR (Score:4, Funny)

    by girlintraining ( 1395911 ) on Sunday September 01, 2013 @12:52AM (#44728695)

    he gene the researchers focused on is called mTOR and is

    ... That gene is no longer available. It was seized by the NSA and is being held in guantanamo bay for suspected ties to drug dealing and terrorism because it may somehow be related to the Tor privacy network.

  • by amaurea ( 2900163 ) on Sunday September 01, 2013 @05:09AM (#44729621) Homepage

    Experiments to breed fruit flies for longevity by only letting them breed after a certain age has produced flies which lived three times as long as normal, if I recall correctly. These had much the same symptoms as the mice: Stronger and more active, even after normal fruit flies would be dead. But with significantly reduced metabolism. This is also similar to how humans who live on a diet that is on the verge of starving them also seem to live longer, but have lower metabolism.

    So lowering the metabolism, and making the cells live in slow motion, essentially, seems to be the easiest way to increase life span. But I think it is a boring dead-end in that there is a limit to how much the metabolism can be lowered, and it does not really solve any of the real issues with old age, such as failing repair mechanisms, lack of new cells, telomer limits vs. cancer, etc.

  • But are they 20% happier?
  • like anything else, the process of aging must also revolve around the imperfect cell replication process that we undergo over time.

    Between pollutants, radiation, etc.. Our cells do NOT replicate perfectly, thus, at some point, the quality of our cells deteriorates, which must be a factor to consider when aging comes to mind.

    As we age from newborn to child to teen to adult hood, perhaps whatever triggers our growth at some point, also proivdes our cells protection and when that goes away, then the cell r
  • I don't want my pesky mice to live 20% longer. I want my cat to kill the b**gers.
  • Trying to prevent aging by tinkering with our enormously complex biological process, is likely to cause many more problems the body that we don't know of. It will likely work for some people while creating all sorts of problems for all the others. With the SENS approach, on the other hand, it's not about changing the biological process to prevent the aging, but rather trying to repair the damage caused by the 7 known cause of aging, with regenerative medicine and other therapies.
  • As a cat I can confidently state that all of Domestic Felineness would welcome these new, slow mice, with open paws. When will these be introduced into the wild?

If graphics hackers are so smart, why can't they get the bugs out of fresh paint?