In glaucoma, should enthusiasm about neuroprotection be tempered by the experience obtained in other neurodegenerative disorders?

Some in nitro and in vivo evidence, as well as rare observations in human e yes with glaucoma, suggests that retinal ganglion cells could be lost by ap optosis during the course of glaucomatous optic neuropathy. There exist als o observations indicating that in the vitreous of patients with glaucoma it is possible to measure an increased concentration of glutamate (an excitot oxic amino acid known to induce neuronal apoptosis in animal models). These observations, among others, suggest the possibility of an excitotoxicity m echanism in the pathogenesis of glaucoma and as a consequence the potential for a neuroprotective approach to treating this disorder. Amazingly, not o nly in glaucoma but also in other neurodegenerative disorders (Parkinson's disease, amyotrophic lateral sclerosis, stroke, etc.) it has been postulate d that neurons could be lost through an excitotoxic mechanism. In these non glaucomatous disorders, quite a large number of clinical trials have alread y been conducted to determine the potential benefit of different neuroprote ctive therapies. Unfortunately, with a few rare exceptions, the results of these clinical studies have been very disappointing (in contrast to encoura ging results obtained in preclinical trials). The experience acquired in ot her neurodegenerative disorders should probably be kept in mind when addres sing the question of neuroprotection in glaucoma. In particular, the hope r aised by preclinical studies showing that drugs could have a beneficial eff ect on the survival of retinal ganglion cells should certainly be tempered until such an effect is confirmed by clinical trials conducted in patients with glaucoma.