A drug to slow ageing has taken a step closer after scientists proved they could lengthen the lifespan of animals by up to 35 per cent.
Researchers at the Mayo Clinic have been studying senescent cells, the name for cells that no longer divide and can accumulate in the body with age, causing damage and disease.
Senescent cells are important because they prevent cancer spreading by stopping cell division and when people are young they are regularly cleared out of the body before they can cause problems.
But as we age the body stops being able to get rid of the dead cells as quickly and they can build up, stopping new cells regenerating.
Now scientists have shown that mice who received a special compound to clear out the senescent cells lived 35 per cent longer than those allowed to age normally. They were also stronger and healthier for longer.
If the same effects could be replicated in humans it could mean people living for decades longer, and in much better health.
First author Dr Darren Baker, a molecular biologist at Mayo Clinic, is optimistic about the potential implications for humans.
“The advantage of targeting senescent cells is that clearance of just 60-70 percent can have significant therapeutic effects,” he said.
“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.”
The results, which appear in the journal Nature show that the clearance of senescent cells also delays tumour formation, preserves tissue and organ function, and extends lifespan without any adverse effects.
The mice also looked healthier and had less inflammation in fat, muscle and kidney tissue.
“Cellular senescence is a biological mechanism that functions as an ’emergency brake’ used by damaged cells to stop dividing,” says Dr Jan van Deursen, Chair of Biochemistry and Molecular biology at Mayo Clinic, and senior author of the paper.
“While halting cell division of these cells is important for cancer prevention, it has been theorized that once the ’emergency brake’ has been pulled, these cells are no longer necessary.
The immune system sweeps out the senescent cells on a regular basis, but over time becomes less effective.
Senescent cells damage adjacent cells and cause chronic inflammation, which is closely associated with frailty and age-related diseases.
Researchers used a compound called AP20187 to trigger genes into ramping up their removal of senescent cells.
“Senescent cells that accumulate with aging are largely bad, do bad things to your organs and tissues, and therefore shorten your life but also the healthy phase of your life,” says Dr. van Deursen.
“And since you can eliminate the cells without negative side effects, it seems like therapies that will mimic our findings – or our genetic model that we used to eliminate the cells – like drugs or other compounds that can eliminate senescent cells would be useful for therapies against age-related disabilities or diseases or conditions.”
Other scientists are also working towards anti-ageing therapies and a trial in the US to test the diabetes drug metformin are due to start later this year.
Prof Ilaria Bellantuono, Professor of Musculoskeletal Ageing, University of Sheffield, said: “This work is interesting because it confirms some of the findings from a previous study, which used mice with accelerated ageing, using mice which are ageing naturally. It shows improved health in some aspects of their ageing such as reduced incidence of cancer, cataracts, and improved memory, suggesting that removal of these aged cells can be beneficial.
“However, it is far from being the solution to healthy ageing as there are several aspects such as mobility which are not improved – and of course this research is in mice, not humans.”