Findings of research undertaken at the University of California, San Diego (UCSD) show that genetic interaction may prove to be a key component in the development and progression of glaucoma. Although the genetic research has been conducted with mice, the findings suggest a possible new target for glaucoma therapy and development of new drugs.

In the most common form of glaucoma, primary open-angle glaucoma (POAG), increased intraocular pressure can lead to the gradual death of retinal ganglion cells, which, if left untreated can cause blindness. Current topical therapies are mainly based around pressure lowering agents, and in some cases surgery may be necessary to reduce the intraocular pressure.

In the UCSD study, researchers looked at the gene variants involved in POAG, identifying them as SIX6 and P16INK4a. SIX6 is required for proper eye development, and P16INK4a irreversibly arrests cell growth, a phenomenon called senescence.

The researchers report that in glaucoma SIX6 and/or intraocular pressure boost the expression of p16INK4a, which in turn accelerates senescence and death of retinal ganglion cells. The findings suggest that inhibiting p16INK4a could offer a new therapeutic approach for glaucoma.

Image: National Eye Institute – flickr – surgery to treat glaucoma