Senescent non-dividing cells of all types accumulate in various tissues. This is probably an adaptation that acts to suppress cancer risk, but these cells secrete damaging compounds that degrade nearby tissue function and cause surrounding cells to also tend towards senescence. The most straightforward approach to removing this contribution to degenerative aging is some form of targeted destruction of senescent cells, perhaps via adaptation of any one of the numerous cell killer technologies under development in the cancer research community.
In recent years some progress has been made in another direction, that of reversing the senescent state of cells. Ultimately the research community will be able to reprogram any cell into any desired state, but that lies a way into the future yet. Reversing senescence will undoubtedly prove complicated and tissue-specific, and there is the open question of whether this will increase cancer risk. Here is an example of one small step on this road, but note that it is only restoring the ability of one type of senescent cell to divide once more. It may or may not be adequately addressing the other undesirable behaviors of the cells, and may or may not turn out to be the best approach.
As we age our immune systems decline. Older people suffer from increased incidence and severity of both infections and cancer. In addition, vaccination becomes less efficient with age. In previous [work, researchers] showed that ageing in immune system cells known as T lymphocytes was controlled by a molecule called p38 MAPK that acts as a brake to prevent certain cellular functions. They found that this braking action could be reversed by using a p38 MAPK inhibitor, suggesting the possibility of rejuvenating old T cells using drug treatment.
In a new study [the] group shows that p38 MAPK is activated by low nutrient levels, coupled with signals associated with age, or senescence, within the cell. It has been suspected for a long time that nutrition, metabolism and immunity are linked and this paper provides a prototype mechanism of how nutrient and senescence signals converge to regulate the function of T lymphocytes. The study also suggests that the function of old T lymphocytes could be reconstituted by blocking one of several molecules involved in the process.
"Our life expectancy at birth is now twice as long as it was 150 years ago and our lifespans are on the increase. Healthcare costs associated with ageing are immense and there will be an increasing number of older people in our population who will have a lower quality of life due in part to immune decline. It is therefore essential to understand reasons why immunity decreases and whether it is possible to counteract some of these changes. An important question is whether this knowledge can be used to enhance immunity during ageing. Many drug companies have already developed p38 inhibitors in attempts to treat inflammatory diseases. One new possibility for their use is that these compounds could be used to enhance immunity in older subjects. Another possibility is that dietary instead of drug intervention could be used to enhance immunity since metabolism and senescence are two sides of the same coin."