The enzyme calcineurin contributes to retinal ganglion cell death, but the drug FK506 inhibits the death of these cells, according to preliminary results of an ongoing study at the Massachusetts Eye and Ear Infirmary.

In glaucoma, we know that the disease progresses because the retinal ganglion cells die, says Cynthia L. Grosskreutz, M.D., Ph.D., co-director of the Glaucoma Service at the Massachusetts Eye and Ear Infirmary.

Our goal is to figure out what mechanisms govern this death and to develop a strategy for protecting the cells from the things that cause them to die, she says.

The study results suggest that calcineurin activation and cleavage may play an important role in glaucomatous optic nerve degeneration. We used animal models of glaucoma to identify calcineurin as a contributor to retinal ganglion cell death in experimental glaucoma, Dr. Grosskreutz says.

The results point to a specific molecular target in retinal ganglion cells that may be amenable to therapeutic intervention. We were able to use the drug FK506 to inhibit calcineurin and observed significant protection of the optic nerve and retinal ganglion cells, she says.

Better understanding of how and why the retinal cells die can help us develop better treatments for this disease, Dr. Grosskreutz says.