Researchers at the Mayo Clinic have managed to extend the lifespan of mice by as much as 35 percent, by clearing out their old, or senescent cells. Though there is much work to do before this technique can be applied to humans, the study provides a significant platform for developing new anti-aging treatments, as it confirms the role that senescence plays in this process.

Senescence refers to the process whereby cells stop dividing. It is caused by a number of factors, including the general wear and tear of the cell's genetic material that occurs with each successive division. Once certain protective sequences of DNA – called telomeres – shorten to a certain point, chromosomes are left vulnerable to damage and thus cells are prone to becoming cancerous.

At this point, the expression of a gene called p16INK4a effectively shuts these cells down, and is therefore an important biological defence mechanism against cancer. However, rather paradoxically, senescent cells also secrete certain compounds that are associated with the development of tumours and drive cellular aging processes. To limit these negative effects, the body’s immune system regularly eliminates senescent cells, although as this process becomes less efficient over time, these cells tend to build up around the body.

To test the effect of removing these cells on overall health, scientists used a compound called AP20187 to target and destroy p16INK4a-expressing cells in mice. Publishing their results in the journal Nature, they explain how this treatment was applied to one-year-old mice, as this represents the approximate mid-point in their lifespan, after which senescent cells tend to build up in greater numbers.

Astonishingly, these mice were found to live an average of 17 to 35 percent longer than those who did not receive the treatment, suggesting that removing senescent cells can slow down the aging process.

The health of these mice was found to be greatly superior to those in the control group, in a number of ways. For example, by scanning the rodents’ hearts, the researchers noted a reduction in mass of the ventricles in the control mice at 18 months old, but not for those whose senescent cells had been eliminated. They therefore conclude that senescence is a key driver of heart disease.

Other age-related health issues, such as fat loss, tumour development, cataracts, and kidney scarring were all found to occur much later in mice who had been treated than those who hadn’t, suggesting that senescence plays a key role in a range of processes associated with aging.

In a statement, lead study author Darren Baker said he now hopes to see this research used to develop new drugs to eliminate senescent cells in humans, which he claims could have “profound impacts on healthspan and lifespan.”