Background. Glaucoma is an optic neuropathy where retinal ganglion cells (R
GC) are lost. It is postulated that this is due to apoptosis, a genetically
regulated cell death mechanism that can potentially be modulated by drugs.
Method. A non-exaustive review of the literature related to the potential o
f neuroprotection to prevent RGC loss in glaucoma.
Results. There exists preclinical evidence, as well as rare observations in
humans, suggesting that RGC could be lost by apoptosis in glaucoma. Potent
ial stimuli that could trigger RGC apoptosis are interruption of axoplasmat
ic flow, generation of reactive oxygen species, nitric oxide-induced toxici
ty and glutamate-induced excitotoxicity. in animal models of glaucoma the p
ossibility of preserving RGC loss by neuroprotective drugs is supported by
many encouraging observations. However, as yet, no clinical studies have ch
allenged this issue in humans. Only recently has such a clinical trial been
initiated.
Conclusions. The concept of neuroprotection in glaucoma makes sense, howeve
r clinical evidence is still lacking.