How one day we may all be eternally young

Growing old may not be mandatory after all. Failing eyesight, loosened teeth and greying hair could be driven by regulatory genes that determine when it is time to shuffle off our mortal coil, rather than being indicators of the ravages of age.

American scientists have challenged the conventional view that ageing is caused by wear and tear – like rust on an old car. Instead, they suggest specific genetic instructions drive the process. If they are right, science might one day find ways of switching the signals off and halting or even reversing ageing.

Researchers at Stanford University Medical Centre raised questions about the conventional theory of ageing on the basis of observations in the animal world. Stuart Kim, a professor of developmental biology, said: "Everyone has assumed we age by rust. But how do you explain animals that don't age?" Some tortoises lay eggs at the age of 100, there are whales that live to be 200 and clams that make it past 400 years, he said.

Those species use the same building blocks for their DNA, proteins and fats as humans, mice and nematode worms. But the chemistry of the wear-and-tear process, including damage from free radicals, should be the same in all cells, which makes it hard to explain why species have dramatically different life spans. "A free radical doesn't care if it's in a human cell or a worm cell," Professor Kim added.

To answer the puzzle, Professor Kim and colleagues studied the nematode worm, one of the most primitive living creatures, and found differences between young and old worms that did not match the conventional picture of ageing. The worms are a millimetre long, age rapidly and have a maximum lifespan of only two weeks. Comparing young and old worms, the scientists found higher levels of three "transcription factors" – molecular switches that turn genes on and off – as they aged.

To see whether these molecules were part of the wear-and-tear ageing process, the researchers exposed the worms to stresses thought to cause ageing such as heat, free-radical oxidation, radiation and disease. None of these affected the genes, suggesting that ageing was not caused by chemical damage. Instead, the results showed that key genetic mechanisms designed for youth had drifted off track in older animals.

Evolution by natural selection cannot weed out problems that occur late in an animal's lifespan, so the genetic pathways for ageing appear to have become entrenched by accident, the researchers said. They called the process "developmental drift" in their findings, which are published in the journal Cell.

Professor Kim said: "We found a normal developmental programme that works in young animals, but becomes unbalanced as the worm gets older. It accounts for the lion's share of molecular differences between young and old worms." If ageing is not a cost of unavoidable chemistry, but is instead driven by changes in regulatory genes, the ageing process may not be inevitable, he added.

Marc Tatar, of Brown University on Rhode Island, said: "The message of this research is that ageing can be slowed and managed by manipulating signalling circuits within cells. This is a new and potentially powerful circuit that has just been discovered for doing that."