The majority of cells in the body can only make a finite number of divisions. This upper bound, called the Hayflick limit, is essential in minimising the random statistical noise that causes incorrect copying of genetic information and leads to mutation and cancer.
However, the cells that can no longer divide, called senescent cells, accumulate over time. They secrete inflammatory molecules called cytokines that cause damage to neighboring tissues, triggering illness, inflammation and contributing to the symptoms of frailty associated with aging.
It is more old-age frailty, and not necessarily our current lifespan, that would be targeted by successful treatment of senescence. As Professor Lynne Cox of Oxford University says “Targeting senescence is about targeting the things that make old age such a misery for so many people. On top of the aches and pains, Alzheimer’s disease, Parkinson’s and multiple sclerosis all have causal links to senescent cells. Improving lifespans is an incredibly admirable goal, but our healthspans should move in pace with this change if we really wish to extract the most value from living longer.”
Senescence is a complex (and not entirely detrimental) process, however. It is an important component in the early stages of our development and in our bodily abilities to suppress cancer and heal wounds. Effective treatment will not just be treatment that solves the problems, then, but will be carefully tailored so as to not remove any benefits.
“The key,” says Prof Cox, “is in finding the right places to treat and the right times to treat them. Early anti-senescence treatment may impair development but catch it too late and the effects are already upon you!”
Like most successes in life – it’s all in the timing.