Slashdot Mirror
Changing a Single Gene Allows Mice To Live 20 Percent Longer
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.'"
at least for now...
"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 assume that extending life is a totally new feature... not a bugfix.
Talk about a gray moment here. For some reason, I thought the headline said Makes Mice 20% Cooler.
This space unintentionally left blank.
...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.
How do we measure mouse posture? They stand up straighter?
if I were a mice this would mean something.
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.
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!"
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.
References:
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.
And then have mice live forever !! Who would not want that !!
Now to help people die faster so that I don't have to work until I'm 100 before I can retire.
In outer space, bone strength is not needed. There are much less foreign organisms for the immune system to deal with. The radiation is going to give you cataracts anyways. So, the rich people can go into outer space, get lots of eye surgery, and live longer.
Or a repressive protein that blocks the operating cells?
Give me quality please.
Im a programmer. I don't need an immune system capable of NYC subway system. I don't need exceptionally strong bones when i'm 60.
What i do need is very good mental health, though.
We want mice to have shorter live, not live longer!
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.
#fuckbeta #iamslashdot #dicemustdie
So, having no mouse wife increases life expectancy?
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?
Mamalian targets for rapamycin down regulation slows down metabolism and disrupt immune system not sure if longer life span is worth it?
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 replication becomes compromised, which means that perhaps there is a mechanism within ourselves as we age into adult hood which protects our cells, once we've gotten to our final stage, we lose this protection and slowly our cells replication process becomes compromised with time and more vulnerable to external factors.
It could be that to really slow down the aging process, we need to better filter what we consume and we need to increase our skin's ability to better shield ourselves from radiation, etc..
I don't want my pesky mice to live 20% longer. I want my cat to kill the b**gers.
On y va, qui mal y pense!
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?