This year saw a demonstration showing noteworthy benefits to health and longevity from the targeted destruction of senescent cells in mice - an expected result for many researchers, but one that had yet to happen up to that point. Senescent cells, cell that have removed themselves from the cycle of proliferation, are an evolutionary response to the growing threat of cancer with age, but once in a senescent state they progressively cause harm to surrounding cells and tissue. The immune system destroys many senescent cells, but becomes much worse at this task - along with all its other duties - as time progresses because it suffers from its own age-related issues. As the numbers of senescent cells grow, so does their contribution to the physical failures and declines of aging.
But this entire portion of the basis for degenerative aging could be removed with a therapy that destroyed senescent cells sufficiently well. This is why the earlier mentioned demonstration of senescent cell destruction - and corresponding health benefits - in mice was a welcome advance. Unfortunately, the method used was based on some clever genetic engineering and while effective at eliminating senescent cells without harming other cells in the engineered mouse breed, it has little direct application to the development of human clinical medicine.
Meanwhile, the cancer and immunotherapy research communities are making great strides in developing many forms of nanoscale technology that can be coupled to a sensor and sent to destroy those cells that the sensor reacts with - and without harming any other nearby cells. Researchers have used nanoparticles, antibodies, viruses, and bacteria to home in on cells with specific surface markers or other characteristics, and there deliver some form of killing blow. The trick here is not so much the killing blow, as many of the successful demonstrations of targeted cancer cell destruction did no more than deliver old-style chemotherapy drugs - just in very small doses and on a cell-by-cell basis rather than flooding the whole body. That works very well to minimize side-effects and maximize harm to the cancer.
The point of this sidebar is that these technology platforms could be quickly repurposed to attack senescent cells, but only when there emerges a robust way of distinguishing between senescent and non-senescent cells. So now we watch with interest for published research that touches on that topic, such as this recent open access paper:
Changes in the shape of the nuclear lamina are exhibited in senescent cells, as well as in cells expressing mutations in lamina genes. To identify cells with defects in the nuclear lamina we developed an imaging method that quantifies the intensity and curvature of the nuclear lamina. We show that this method accurately describes changes in the nuclear lamina. Spatial changes in nuclear lamina coincide with redistribution of lamin A proteins and local reduction in protein mobility in senescent cell. We suggest that local accumulation of lamin A in the nuclear evelope leads to bending of the structure. A quantitative distinction of the nuclear lamina shape in cell populations was found between fresh and senescent cells, and between primary myoblasts from young and old donors. Moreover, with this method mutations in lamina genes were significantly distinct from cells with wild-type genes. We suggest that this method can be applied to identify abnormal cells during aging, in in vitro propagation, and in lamina disorders.
As an aside, you might recall that mutant lamin A is the culprit in progeria, and has been postulated to be a low-level contribution to normal aging as well. Expect to see more interest in progeria and potential therapies for that condition if more evidence emerges to link it to cellular senescence and ways to reliably distinguish senescent cells.