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Editors Selection IGR 9-1

Basic research: Investigative neuroprotection

Comment by Michal Schwartz on:

11698 Effect of glatiramer acetate on primary and secondary degeneration of retinal ganglion cells in the rat, Blair M; Pease ME; Hammond J et al., Investigative Ophthalmology and Visual Science, 2005; 46: 884-890

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In their attempt to confirm the protective effect of glatiramer acetate (GA) on secondary degeneration of RGCs in the rat, using a model of a partial transection developed in the laboratory of Harry A. Quigley,¹ Blair et al. (83) found, in agreement with the finding of Yoles et al.,² that injury to the optic nerve results in secondary degeneration. Using their model to test the effect of GA, however, they obtained negative results, and concluded that "there is no evidence that GA has a neuroprotective effect after optic nerve transection, either for primarily injured or secondarily involved RGC." It is unfortunate that the study lacks a positive control, which is a critical requirement for validation of a negative outcome in any experimental paradigm. Thus, because the authors have not shown that in their model retinal ganglion cells can be protected by any compound at all (including compounds found to be neuroprotective in any model of injury to the visual system), there is no way to rule out the possibility that their negative findings reflect a limitation of the model and not the efficacy of the tested treatment. Yet, even with that caveat their conclusion cannot be justified. In discussing their negative results the authors claim that they repeated the protocol used by other groups to show that GA is protective. In fact, while resembling the protocol used in a study by Kipnis et al. in a rat model of partial crush injury of the optic nerve or of elevated IOP,^3,4 the protocol used in the Quigley study was different. The percentage of microbacteria in their adjuvant was 2.5-fold higher than in that study, and the amount of microbacteria has been shown to critically affect the outcome.⁵ Moreover, while their conclusion might be correct in the case of the model they used, there is no justification for viewing that model as the ultimate model for secondary degeneration and assuming that their finding is generally applicable. This reservation is especially relevant in view of the large body of literature reporting that GA is neuroprotective in a variety of models.^4,6-8 Therefore, their concluding sentence should end with the words "in our model."

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