Lingering populations of senescent cells grow with age, and cause considerable harm via their inflammatory secretions. They are a tool to promote regeneration and resistance to cancer in the short term, but like many short term systems, they become damaging when left switched on for the long term. As I noted just yesterday, even looking at only the past year of studies of senolytic therapies to selectively destroy senescent cells, there is strong evidence in animal models for their ability to prevent or reverse a score of common age-related conditions, a broad range from Alzheimer's disease and other forms of neurodegeneration to fibrosis of the heart and kidney. This is just a starting point. Senolytics have yet to be tested in earnest for many more conditions that could plausibly be reversed by the targeted removal of senescent cells; there is only so much funding, and only so many scientists.

As the study of senescent cells in the context of aging expands, with the continued influx of new funding driven by a growing interest in this part of the field, we should expect to see ever more examples such as the one I'll note today. This is yet another age-related condition with poor treatment options in which animal models are shown for the first time to benefit from the application of senolytics.

In this case the condition is glaucoma, loss of vision caused by degeneration of retinal ganglion cells and the optic nerve. In most cases - but not all - this is caused by increased pressure in the eye, driven by hypertension and degeneration of fluid channels responsible for draining the eye. The precise nature of the relationship between risk factors such as pressure and mechanisms of neural degeneration in the eye has been far from clear, unfortunately. In this context, it is a ray of hope that the research here demonstrates cellular senescence as an important mediating mechanism, showing that removal of these cells prevents half of the retinal ganglion cell death that is produced in a model of raised pressure in the eye.

Early removal of senescent cells protects retinal ganglion cells loss in experimental ocular hypertension