Purpose: Research on the mechanism of cell death in experimental glauc
oma indicates that ganglion cells die by apoptosis. Several stimuli ma
y account for the activation of apoptosis in glaucoma, including neuro
trophin deprivation caused by blockage of retrograde axonal transport
during periods of elevated IOP, or glutamate toxicity caused by ischem
ia to the optic nerve and ganglion cells. Results: The finding that ap
optosis is a significant mechanism of cell death in glaucoma may make
it possible to develop new treatments that specifically block or inter
fere 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 t
he disease and not the cause. Still, in many cases ganglion cell death
has already been stimulated in patients by the time they are diagnose
d with glaucoma and continues to progress even after conventional trea
tments. Conclusion: Thus, therapies that prevent further ganglion cell
death, in combination with standard pressure management therapies, ma
y become a viable treatment for glaucoma in the future.