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Editors Selection IGR 13-2

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Comment by Robert Casson on:

22579 Effect of brimonidine on retinal ganglion cell survival in an optic nerve crush model, Ma K; Xu L; Zhang H et al., American Journal of Ophthalmology, 2009; 147: 326-331

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Optic nerve damage caused by acute injury or diseases such as glaucoma is associated with progressive retinal ganglion cell death resulting in impaired vision and blindness. The quest for drugs to enhance retinal ganglion cell survival is ongoing and brimonidine, a α2-adrenergic agonist, has recently been shown to exert a neuroprotective effect in a rat chronic ocular hypertension model.
The study by Ma and co-workers examines the effects of intraperitoneal injections of brimonidine on retinal ganglion cell survival four weeks after optic nerve crush in adult rats. The authors report a neuroprotective effect of brimonidine treatment, and suggest that brimonidine may be neuroprotective in a variety of optic nerve damage models.
Whilst this is an interesting observation, further clarification of a number of issues would be helpful. Optic nerve crush is generally associated with high levels of retinal ganglion cell death. Previous studies have reported that three weeks after optic nerve crush the majority of retinal ganglion cells have died. In contrast, Ma et al., using a similar optic nerve crush model and even longer timeframe, report a survival rate of around 53.5 % in saline treated controls, which rose to 61% of retinal ganglion cells surviving after brimonidine treatment. Whilst this appears to be a promising neuroprotective trend, the magnitude of the effect is quite small. Indeed, it is mainly the impressively low variability in axonal loss within each group that makes the effect detectable with the relatively small number of animals used. It is also uncertain if the protective effect is sustained in a clinically useful way, as only one time point was studied. Is this delayed death or true protection?
It is also unclear how a neuroprotective effect of systemically administered brimonidine could be mediated. It has been suggested that brimonidine may exert its neuroprotective effects by increasing neurotrophic factor expression, but there is relatively little evidence for this in vivo. Further studies on the mechanisms how brimonidine exerts its proposed neuroprotective effects will be of great interest.

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