UMass asks: Could genes code for 'healthspan'?
Researchers at the University of Massachusetts Medical School in Worcester are wondering if studies of a lowly worm can help us understand how to better maintain health as we age.
Findings on the genetically altered nematode species C. elegans showed that, compared with typical nematodes, the long-lived mutant worms spend a greater portion of their life in a frail state and exhibit less activity.
The research, published in “Proceedings of the National Academy of Sciences,” suggests that genes that extend lifespan won’t necessarily improve health in advanced age, and points to the need to measure health as part of aging studies, a news release this week from the school said.
Scientists have identified several groups of genes that control longevity in C. elegans, used as a model system for genetic studies. However, studies have usually been done on young nematodes, neglecting the latter portion of the animals’ lives, the statement from UMass said.
UMass researcher Heidi A. Tissenbaum and her colleagues sought to investigate how healthy long-lived C. elegans mutants were as they aged. She said her team “set out to create a definition of ‘healthspan’ by identifying traits that could be easily verified and measured as the worms aged.”
“Our study reveals that if we want to find the genes that help us remain physically active as we age, the genes that will allow us to play tennis when we’re 70 similar to when we were 40, we have to look beyond longevity as the sole criteria. We have to start looking at new genes that might play a part in ‘healthspan,’ ” said Tissenbaum, professor of molecular, cellular and cancer biology and the molecular medicine program at UMass Medical School.
While the UMass researchers found some extension in health as the mutants aged for certain traits, as a whole “the tradeoff was an extended period of frailty and inactivity,” she said in the statement. “In fact, as a percentage of total lifespan, the wild-type worms spent more time in a healthy state than the long-lived mutants.”
The implication for scientists, according to Tissenbaum, is that the set of genes that influence longevity may be distinct from the genes that control healthspan. “This study suggests that there is a separate and unexplored group of genes that allow us to perform at a higher level physically as we age. When we study aging we can no longer look at lifespan as the only parameter; we also have to consider health as a distinct factor of its own.”
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