Washington, Mar 13 : Researchers at the University of Washington and other institutions have found 25 longevity genes present in two organisms that are 1.5 billion years apart in evolutionary change.
The research led by Brian Kennedy, UW associate professor of biochemistry, also indicated that almost 15 of those gene variants are present in humans and may have future implications in targeting those genes to help slow down the aging process and treat age-related conditions.
The two organisms used in this study, the single-celled budding yeast and the roundworm C. elegans, are commonly used models for aging research.
According to the researchers it is important to find genes that are conserved between the two organisms, because the two species are so far apart on the evolutionary scale -- even farther apart than the tiny worms and humans. Besides, presence of similar human genes is an indication that these genes could regulate human longevity also.
"Now that we know what many of these genes actually are, we have potential targets to go after in humans. We hope that in the future we could affect those targets and improve not just lifespan, but also the 'health span' or the period of a person's life when they can be healthy and not suffer from age-related illnesses," said Kennedy.
As suggested by earlier evolutionary theories, aging was not genetically controlled, since an organism does not get any advantage in natural selection by having a very long lifespan that goes far past their reproductive age.
With an aim to find these lifespan-controlling genes, the scientists followed a genomic approach to carefully examine genes that affect aging in yeast and worms. They first identified 276 genes in C. elegans that affected aging, and then looked for similar genetic sequences in the yeast genome. Among the 25 aging-related genes found in both worms and yeast, only three had been previously thought to be conserved across many organisms.
It was found that many genes identified to be involved in aging are also connected to a key nutrient response pathway known as known as the Target of Rapamycin, or TOR. This may provide more evidence to the theory that calorie intake and nutrient response affect lifespan by altering TOR activity.
According to earlier studies, drastic restriction of caloric intake of organisms, an approach known as dietary restriction, can extend their lifespan and reduce the incidence of age-related diseases. TOR inhibitors are being tested clinically in people for anti-cancer properties, and this work suggests they may also be useful against a variety of age-associated diseases.
"What we'd like to eventually do is be able to mimic the effects of dietary restriction with a drug. Most people don't want to cut their diet that drastically, just so they may live a little longer. But someday in the future, we may be able to accomplish the same thing with a pill," explained Matt Kaeberlein, one of the senior author of the study.
The scientists said that the results of this study also provide new insight into the genetic basis of aging, and provide some of the first quantitative evidence that genes regulating aging have been conserved during the process of evolution.
The study is published online by the journal Genome Research.