For the first time ever, scientists have successfully modified the expression of a particular gene in mice to not only increase their lifespan, but also slow the rate at which they age.

The gene in question, Myc, is common to all animals, and has long been the subject of research after it was found to be responsible for regulating cell proliferation, growth and death. It has even been closely linked to cancer.

Normally animals have two copies of the Myc gene, but researchers from Brown University bred laboratory mice to only have one – the first time anyone has done this in any mammal.

To their surprise, the scientists found that the mice lived longer than their two-Myc counterparts and also aged at a slower rate.

The female mice lived 20% longer, while the male mice lived 10% longer.

“The animals are definitely aging slower. They are maintaining the function of their organs and tissues for longer periods of time,” explained lead study author John Sedivy, the Hermon C Bumpus professor of biology and professor of medical science at Brown University.

What was particularly surprising, however, was the relative lack of adverse effects to the mice.

The animals were around 15% smaller than their normal alternatives, but despite the scientists studying the mice in incredible detail – right down to the molecular level – no other issues were found.

The mice could reproduce just as successfully and behaved completely normally.

“These mice are incredibly normal, yet they are really long-lived,” said Sedivy.

“The reason why we were struck by that is because in many other longevity models like caloric restriction or treatment with rapamycin, the animals live longer but they also have some health issues.”

Instead, these mice had fewer health issues as a result of their slower ageing. They showed no signs of osteoporosis or cardiac fibrosis, had lower cholesterol than normal ageing mice, had better coordination and were generally more active.

While the study was undertaken entirely on mice, the researchers believe that the work could eventually be of benefit to humans.

Most important will be finding the right aspect of the Myc gene to target with drugs.

Sedivy would not confirm that doing this could definitely extend the human lifespan – he said this may or may not be an effect of the correct treatment – but it may well allow people to remain healthier for longer into their lives.

One clear possibility would be to target the gene to prevent osteoporosis, which is a common problem in the elderly.

Alternatively, blocking over-expression of the gene may be key to stopping cancers from developing; something that cancer researchers are already looking at. These new findings may prove highly encouraging for such projects, and may even provide the basis for additional funding in this area.

Journal reference: Cell Vol. 161, doi:10.1016/j.cell.2014.12.016.