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.'"
Re:Blatant conjecture (Score:5, Interesting)
Re:Blatant conjecture (Score:5, Interesting)
Since there are no animals that live forever, you have to assume that extending life is a totally new feature... not a bugfix.
Really? http://www.cracked.com/article_20055_6-unassuming-animals-that-are-secretly-immortal.html [cracked.com]
Hey! Cracked is at least as reliable as CNN, fox, or MSNBC, and lately it is more unbiased.
New Research, Same Problem (Score:3, Interesting)
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.