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Editors Selection IGR 24-3

Basic research: Neuroprotection and minocycline

Comment by Harry Quigley on:

21029 Reduced retina microglial activation and improved optic nerve integrity with minocycline treatment in the DBA/2J mouse model of glaucoma, Bosco A; Inman DM; Steele MR et al., Investigative Ophthalmology and Visual Science, 2008; 49: 1437-1446

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In 2006, Levkovitch-Verbin et al. showed that minocycline is a neu-roprotective agent for glaucoma in a well-designed, masked evalu-ation of experimental glaucoma in the rat (Arch Ophthalmol 2006; 124: 520-526). Because this drug is generic, it faces the likelihood that no pharmaceutical company will market it for this indication in humans, this unequivocal demonstration of its effectiveness and its mechanism by suppressing ganglion cell apoptosis was of fundamental impor-tance, since the drug is well tolerated in humans. Bosco et al. (565) have recently reported a follow-up study on minocycline in the spontaneous DBA/2J mouse. A number of problems with the experiment unfortunately limit the significance of the report. 1) Intra-ocular pressure was measured with the TonoPen, which is an inferior method compared to the TonoLab. 2) There was a clear difference in IOP between the minocycline-treated and control animals that was not taken into account in the analysis. 3) Both eyes of animals were included in the analysis without taking interocular correlation into account. 4) Data on axon counts are not actually presented, though from the Figure with individual data, it is clear there was no protection afforded by minocycline. 5) Ganglion cell body counts were done by both NeuN immunolabeling (which showed no protection) and Fluorogold backfilling (which showed a modest protective effect). However, unless the difference in IOP is included in the analysis, this may simply be an IOP-dependent effect that does not indicate the mechanism of minocycline protection. The authors studied microglial numbers in the retina, which were not affected by minocycline, but did not study the same glia in the optic nerve head or optic nerve. They show some differences in ramification of microglia, which may indicate that minocycline affected activation of these glia in the retina. In summary, there is reason to study minocycline as a neuroprotective agent in human trials, though the Bosco et al. Publication adds little to the rationale.

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