SUMMARY
Glaucoma is often associated with high intraocular pressure (lOP), but continues to progress even after normalization of IOP. We have suggested that such progression is at least partly due to delayed degeneration of spared neurons by their exposure to the degenerative milieu created by degenerating neurons, the primary victims ofhigh IOP. The extent of delayed (secondary) degeneration is apparently a function of the severity of the primary insult, which affects the level of toxicity mediators and the spared neurons’ susceptibility to them. We developed a model of adult rat partial optic nerve lesion to quantify the extent of primary and secondary damage, respectively, and find out why patients with severe pre-existing damage are more prone to deterioration than patients without pre-existing visual loss. The model also screens compounds for neuroprotective efficacy. Our findings support our suggestion that glaucoma therapy should consist of a combination of neuroprotection and ocular hypotensive therapy.
Keywords:
Glaucoma; Neuroprotection; Optic nerve injury