Bansal A, Zhu LJ, Yen K, Tissenbaum HA.
Uncoupling lifespan and healthspan in Caenorhabditis elegans longevity mutants.
Proc Natl Acad Sci U S A. 2015 Jan 5;
PubMed.
A good argument can be made that the best way to reduce the burden of age-associated neurological diseases such as Alzheimer's would be to slow the rate of aging itself. The existence of single gene mutations that significantly extend the lifespan of model organisms (worms, flies, and mice) suggests that aging is malleable to some degree, making anti-aging treatments potentially both feasible and desirable. A nagging concern, however, is the possibility that lifespan could be increased without a concomitant increase in healthspan, which could lead to an actual increase in the number of older people suffering from age-associated diseases. The recent study by Bansal et al. takes a careful look at the relationship between healthspan and lifespan in the nematode worm C. elegans. In this study, populations of worms with single gene mutations that increase lifespan were carefully followed throughout their lifespan and assayed for reasonable surrogates of worm health: movement and resistance to stress. While some mutations did show an increased healthspan for some measurements, the strong trend was that healthspan did not track lifespan, and discouragingly, all of the mutations increased the period for which the worms were measurably frail.
Will this result translate to people? Children of long-lived parents have been reported to have lower rates of Alzheimer's disease (Lipton et al., 2010), and anecdotally, centenarians appear to have been significantly healthier in their 80s than contemporaries who were not destined to live as long. It is also somewhat unclear what extended lifespan means in C. elegans worms: They appear to stop eating long before they actually die, and it is not actually known what aged worms die "from" (clearly not cancer, heart disease, or stroke). Nevertheless, this study clearly demonstrates that, at least in one well-studied model, lifespan can be disassociated from healthspan. These results emphasize the importance of following health measurements both in model organism studies and attempts to develop anti-aging treatments in people (Seals and Melov, 2014).
References:
Lipton RB, Hirsch J, Katz MJ, Wang C, Sanders AE, Verghese J, Barzilai N, Derby CA.
Exceptional parental longevity associated with lower risk of Alzheimer's disease and memory decline.
J Am Geriatr Soc. 2010 Jun;58(6):1043-9. Epub 2010 May 7
PubMed.
Seals DR, Melov S.
Translational geroscience: emphasizing function to achieve optimal longevity.
Aging (Albany NY). 2014 Sep;6(9):718-30.
PubMed.
Comments
University of Colorado
A good argument can be made that the best way to reduce the burden of age-associated neurological diseases such as Alzheimer's would be to slow the rate of aging itself. The existence of single gene mutations that significantly extend the lifespan of model organisms (worms, flies, and mice) suggests that aging is malleable to some degree, making anti-aging treatments potentially both feasible and desirable. A nagging concern, however, is the possibility that lifespan could be increased without a concomitant increase in healthspan, which could lead to an actual increase in the number of older people suffering from age-associated diseases. The recent study by Bansal et al. takes a careful look at the relationship between healthspan and lifespan in the nematode worm C. elegans. In this study, populations of worms with single gene mutations that increase lifespan were carefully followed throughout their lifespan and assayed for reasonable surrogates of worm health: movement and resistance to stress. While some mutations did show an increased healthspan for some measurements, the strong trend was that healthspan did not track lifespan, and discouragingly, all of the mutations increased the period for which the worms were measurably frail.
Will this result translate to people? Children of long-lived parents have been reported to have lower rates of Alzheimer's disease (Lipton et al., 2010), and anecdotally, centenarians appear to have been significantly healthier in their 80s than contemporaries who were not destined to live as long. It is also somewhat unclear what extended lifespan means in C. elegans worms: They appear to stop eating long before they actually die, and it is not actually known what aged worms die "from" (clearly not cancer, heart disease, or stroke). Nevertheless, this study clearly demonstrates that, at least in one well-studied model, lifespan can be disassociated from healthspan. These results emphasize the importance of following health measurements both in model organism studies and attempts to develop anti-aging treatments in people (Seals and Melov, 2014).
References:
Lipton RB, Hirsch J, Katz MJ, Wang C, Sanders AE, Verghese J, Barzilai N, Derby CA. Exceptional parental longevity associated with lower risk of Alzheimer's disease and memory decline. J Am Geriatr Soc. 2010 Jun;58(6):1043-9. Epub 2010 May 7 PubMed.
Seals DR, Melov S. Translational geroscience: emphasizing function to achieve optimal longevity. Aging (Albany NY). 2014 Sep;6(9):718-30. PubMed.
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