The rise in number of senescent cells with age is one of the root causes of degenerative aging. Somatic cells become senescent when they reach the Hayflick limit on replication, or become damaged, or encounter a toxic environment. They cease replication, and either self-destruct or are destroyed by the immune system. Some small fraction of the countless cells that become senescent each and every day manage to evade destruction, however. They linger, in ever greater numbers with each passing year, and the potent mix of signal molecules they secrete contributes to many forms of tissue dysfunction and organ failure, ranging from fibrosis and loss of regenerative capacity to increased inflammation and loss of tissue elasticity.

Fortunately, we stand just a few years removed from of the clinical availability of therapies that can destroy some fraction of these cells. A few startup companies are working on senolytic treatments ranging from repurposed chemotherapeutic drugs to gene therapies to antibody therapies. Senolytic treatments that work in humans will literally produce rejuvenation to some degree, turning back one of the causes of aging. They don't even have to be expensive in the case of repurposed drug candidates, though these are unlikely to be as effective as the final results of further development efforts. Indeed, the adventurous can order and use some of these drug candidates even now, and experiment upon themselves, with very little outlay of funds. Caution is always recommended, of course.

Perhaps the most important objection to self-experimentation in the matter of the first legitimate rejuvenation therapies is that there is no readily available measure that will determine just how many senescent cells have been destroyed by a treatment. This is a challenge for formal human pilot trials as well. It means that secondary measures or expensive laboratory work are required, and in a basically healthy individual in middle age, it may well be the case that it is hard to separate out the effects of a crude but legitimate rejuvenation therapy from the noise. Aging has numerous distinct contributing causes, forms of cell and tissue damage that mingle to produce the initially slow decline. It is reasonable to expect it to be hard to see the short-term effect of removing 25% of senescent cells in, say, a 50-something individual who has yet to develop a severe manifestation of any of the age-related conditions most strongly linked to cellular senescence. On the other hand, maybe it will produce meaningful impact in cardiovascular measures such as blood pressure and pulse wave velocity. Without referencing a body of data that doesn't yet exist, it is hard to say which of these is the case.

Measures of senescent cell counts in a living individual would be inarguable, however, assuming they could be carried out without generating injury in the process of obtaining that information, as senescent cells are generated temporarily as a part of the response to wounding. Given such a metric, assessed before and after a treatment, one could definitively say whether or not the treatment achieved the intended result - and then all the uncertainty in secondary benefits achieved at any given age and health status will become more a matter of interesting further research than an outright roadblock. Unfortunately, we don't yet have a useful and broadly available tool to achieve this result. Possibilities include, say, some form of blood sample analysis that looks for the distinctive pattern of signal molecules produced by senescent cells. That is a reasonable research and development project for any group capable of proteomics-based analysis of blood, and perhaps there are people out there working away on it, quietly.

The authors of the open access paper below present an intriguing alternative, and one that might be more easily established and deployed. It is based on the observation that senescent cells are large, some twice as large as normal cells, or even larger. Thus these cells could be filtered from blood via the use of suitably sized fluid channel devices and then counted via flow cytometry, a task that is well-established and business as usual in the microfluidic device industry. Is it reasonable to expect that a higher burden of senescence throughout the body would be more or less accurately reflected by a larger number of senescent cells in the bloodstream? Possibly, but again, the work to prove and quantify all of that has yet to be accomplished. Still, the microfluidics approach to a senescence assay seems a very promising direction for further development.

Senescence chips for ultrahigh-throughput isolation and removal of senescent cells