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Editors Selection IGR 11-2
Basic research: Investigative neuroprotection
Comment by Leonard A. Levin on:
12144 Development and evaluation of psychometric tests of the Chinese-version of low vision quality of life questionnaire, Zou HD; Zhang X; Xu X et al., Chinese Journal of Ophthalmology, 2005; 41: 246-51
Blair et al. (83) describe the lack of effect of glatiramer acetate in protecting against retinal ganglion cell death from partial optic nerve transection with a diamond blade. They used a model which they had previously shown to result in not just death of the immediately transected axons, but also retinal ganglion cells associated with nearby axons. This is a type of secondary degeneration, and theoretically a candidate for neuroprotection. Previously, Michal Schwartz's laboratory had shown that glatiramer acetate, which is used as an immunomodulator for the treatment of multiple sclerosis, stimulates the immune system for neuroprotection of retinal ganglion cells. In contrast, the Blair study, from the Quigley laboratory, did not show neuroprotection. Given that both groups are headed by excellent scientists, the question should be, "What accounts for the differences?" One difference might relate to the lack of oral supplementation, which was used by the Schwartz group for their crush studies, but not in the Blair study. A second difference is how the retinal ganglion cells were counted. A difficulty with counting RGCs in whole-mounts is that microglia, which phagocytose the fluorescent dye used to label the RGC, may be confused with the RGC itself. The Barres laboratory has used BSL-1, a lectin which binds microglia, as a marker for these cells. However, most laboratories simply identify microglia based on their morphology and size. Given that glatiramer acetate is probably acting via the immune system, it is possible that the number and activity of microglia may be affected by treatment. Difficulty or inaccuracy in differentiating microglia from retinal ganglion cells may therefore hide drug effects in models where there are changes in immune activation. Finally, a third difference between the present study and previous studies with glatiramer acetate is the mode of nerve injury. In the present study the injury was with a diamond blade, while in the Schwartz group studies, the injury was crush with calibrated forceps. The former may be less likely to lead to infiltration of macrophages and other immune cells because of its clean and precise nature. If there are less macrophages, then perhaps the effect of immunomodulation may be more difficult to detect.
In summary, the fact that the Blair study has such different results from what was previously published is very useful for stimulating research into how experimental models might have very different consequences for the study of neuroprotection.
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