Purpose: Research on the mechanism of cell death in experimental glaucoma indicates that ganglion cells die by apoptosis. Several stimuli may account for the activation of apoptosis in glaucoma, including neurotrophin deprivation caused by blockage of retrograde axonal transport during periods of elevated IOP, or glutamate toxicity caused by ischemia to the optic nerve and ganglion cells.
Results: The finding that apoptosis is a significant mechanism of cell death in glaucoma may make it possible to develop new treatments that specifically block or interfere with this form of cell death. Preventing ganglion cell death may only be a stop-gap measure, however, in that it treats the result of the disease and not the cause. Still, in many cases ganglion cell death has already been stimulated in patients by the time they are diagnosed with glaucoma and continues to progress even after conventional treatments.
Conclusion: Thus, therapies that prevent further ganglion cell death, in combination with standard pressure management therapies, may become a viable treatment for glaucoma in the future.