A new study has shown that the lifespans of mice can be extended by up to 35 percent by simply clearing out senescent cells - defunct cells that stop dividing, accumulate in old age, and trigger inflammation in fat, muscle, and kidney tissues.

Not only did the mice experience significantly longer lifespans thanks to removal of these cells, but the treatment also delayed the onset of age-related disorders such as heart and kidney deterioration, and the development of cataracts and tumours.

"It's not just that we're making these mice live longer; they actually stay healthier longer too. That's important, because if you were going to equate this to people, well, you don't want to just extend the years of life that people are miserable or hospitalised," one of the team, cell biologist Darren Barker from the Mayo Clinic College of Medicine, told William Herkewitz at Popular Mechanics.

Senescent cells are found all over the body - in our skin, muscles, and organs - and for whatever reason, experienced an unusual amount of stress that caused them to stop dividing, possibly to lower the risk of ending up as cancer cells.

"Cellular senescence is a biological mechanism that functions as an 'emergency brake' used by damaged cells to stop dividing," one of the researchers, Jan van Deursen, said in a press release. "While halting cell division of these cells is important for cancer prevention, it has been theorised that once the 'emergency brake' has been pulled, these cells are no longer necessary."

When we’re young, our immune system regularly clears these stagnant cells out, but as we get older, this function becomes less effective, and they build up and wreak havoc on our health. Accumulations of these cells have previously been linked to heart failure, arthritis, Alzheimer's, and cancer.

To figure out what would happen if this clearing mechanism continued properly into old age, the team genetically engineered mice that would produce a cell-killing protein called caspase in response to another protein called p16, which is only produced by senescent cells. The release of caspase could be triggered and controlled by giving the mice a specific drug, so once they hit middle-age (12 months for mice, which is equivalent to 40 years in humans), they started the treatment. They were given injections twice a week, for the rest of their lives.

While the effects of the senescent cell-clearing weren't immediately apparent, everything changed when the mice hit old age. Reporting in Nature today, the team found that their lifespans were extended by between 17 and 35 percent (with an average of 25 percent), and were much healthier than the untreated, elderly controls.

While the treatment wasn’t perfect - some senescent cells managed to survive, including those in the colon and liver, and wounds actually ended up healing slower than in the controls - there’s a whole lot of potential here.

What the researchers need to do next is figure out a way to safely clear out senescent cells in humans - a whole lot more difficult when you can’t just genetically engineer them to do what you want. But that’s not going to stop researchers from trying to develop drugs that have the same effect in humans.

As Popular Mechanics reports, a new US-based company called Unity Biotechnology stated today that it hopes to use the findings of this study to develop medicines that fight the process of ageing in humans.

"The advantage of targeting senescent cells is that clearance of just 60 to 70 percent can have significant therapeutic effects," said Barker. "If translatable, because senescent cells do not proliferate rapidly, a drug could efficiently and quickly eliminate enough of them to have profound impacts on healthspan and lifespan."

Can't wait to get old and stave off death with you.