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Proc Natl Acad Sci U S A. 2015 Jan 20;112(3):E277-86. doi: 10.1073/pnas.1412192112. Epub 2015 Jan 5.

Uncoupling lifespan and healthspan in Caenorhabditis elegans longevity mutants.

Author information

1
Programs in Gene Function and Expression.
2
Programs in Gene Function and Expression, Bioinformatics and Integrative Biology, and Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605.
3
Programs in Gene Function and Expression, Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605 heidi.tissenbaum@umassmed.edu.

Abstract

Aging research has been very successful at identifying signaling pathways and evolutionarily conserved genes that extend lifespan with the assumption that an increase in lifespan will also increase healthspan. However, it is largely unknown whether we are extending the healthy time of life or simply prolonging a period of frailty with increased incidence of age-associated diseases. Here we use Caenorhabditis elegans, one of the premiere systems for lifespan studies, to determine whether lifespan and healthspan are intrinsically correlated. We conducted multiple cellular and organismal assays on wild type as well as four long-lived mutants (insulin/insulin-like growth factor-1, dietary restriction, protein translation, mitochondrial signaling) in a longitudinal manner to determine the health of the animals as they age. We find that some long-lived mutants performed better than wild type when measured chronologically (number of days). However, all long-lived mutants increased the proportion of time spent in a frail state. Together, these data suggest that lifespan can no longer be the sole parameter of interest and reveal the importance of evaluating multiple healthspan parameters for future studies on antiaging interventions.

KEYWORDS:

functional capacity; gerospan; healthspan; healthy aging; lifespan

PMID:
25561524
PMCID:
PMC4311797
DOI:
10.1073/pnas.1412192112
[Indexed for MEDLINE]
Free PMC Article

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