Neuroprotection in glaucoma. Where is the clinical evidence?

Citation
Io. Haefliger et al., Neuroprotection in glaucoma. Where is the clinical evidence?, OPHTHALMOLO, 98(6), 2001, pp. 564-567
Citations number
20
Categorie Soggetti
Optalmology
Journal title
OPHTHALMOLOGE
ISSN journal
0941293X → ACNP
Volume
98
Issue
6
Year of publication
2001
Pages
564 - 567
Database
ISI
SICI code
0941-293X(200106)98:6<564:NIGWIT>2.0.ZU;2-X
Abstract
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.