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Acta Ophthalmol. 2009 Jun;87(4):450-4. doi: 10.1111/j.1755-3768.2008.01459.x. Epub 2009 Jan 9.

Recent clinical findings with memantine should not mean that the idea of neuroprotection in glaucoma is abandoned.

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1
Nuffield Laboratory of Ophthalmology, John Radcliffe Hospital, Oxford University, Headley Way, Oxford, UK. neville.osborne@eye.ox.ac.uk

Abstract

Loss of vision in primary open-angle glaucoma (glaucoma) is caused by retinal ganglion cells dying at a seemingly steady and variable rate in different patients. Present treatments for all glaucoma patients are inadequate and a goal to rectify this is to discover appropriate drugs or chemicals (neuroprotectants) that can be taken orally to slow down retinal ganglion cell death and have negligible side-effects. It was therefore of great disappointment to learn earlier this year that the one clinical trial conducted to test the efficacy of memantine as a neuroprotectant for glaucoma was unsuccessful. In this article, I consider the mechanisms by which retinal ganglion cells may die in glaucoma and suggest that memantine may have benefited patients taking it but to a level that was difficult to detect with present methodologies. Ganglion cells are induced to die by different triggers in glaucoma, suggesting that neuroprotectants with multiple modes of actions are likely to reveal clearer results than was found for memantine. Therefore, the idea of neuroprotection in glaucoma must not be abandoned.

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