Could you live to be 500? Genetic tweaking in worms helps them live five times longer

LIVING to the ripe old age of 500 might be a possibility if what works for worms can apply to humans, a study has shown.

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LIVING to the ripe old age of 500 might be a possibility if what works for worms can apply to humans, a study has shown.

Experts tweaked two genetic pathways in the tiny lab worm Caenorhabditis elegans and boosted the creature's lifespan by a factor of five.

"What we have here is a synergistic five-fold increase in lifespan," said US lead scientist Dr Pankaj Kapahi, from the Buck Institute of Age Research.

"The two mutations set off a positive feedback loop in specific tissues that amplified lifespan. Basically these worms lived to the human equivalent of 400 to 500 years."

While living for hundreds of years might be a tall order, the research raises the prospect of anti-ageing treatments based on genetic interactions, according to Dr Kapahi.

"In the early years, cancer researchers focused on mutations in single genes, but then it became apparent that different mutations in a class of genes were driving the disease process," he said.

"The same thing is likely happening in ageing."

C. elegans, the first animal to have its whole genome, or genetic code, mapped, has been widely used in studies of ageing and lifespan.

The new research, reported in the journal Cell Reports, involved blocking key molecules that affect the action of insulin and a nutrient signalling pathway called Target of Rapamycin (TOR).

Single mutations in the TOR pathway were known to extend the lifespan of C. elegans by 30 per cent, while insulin-signalling mutations could double the amount of time they lived.

Adding the two together might have been expected to extend longevity by 130 per cent - but the combined impact turned out  to be much greater.

The research may explain why it has proved so difficult to identify single genes responsible for the long lives enjoyed by human centenarians.

"It's quite probable that interactions between genes are critical in those fortunate enough to live very long, healthy lives," said Dr Kapahi.

Future research is expected to use mice to see if the same effects occur in mammals.

"The idea would be to use mice genetically engineered to have suppressed insulin signaling, and then treat them with the drug rapamycin, which is well-known to suppress the TOR pathway," Dr Kapahi added.