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Neuroprotection in the real world
Author(s) -
KURYSHEVA N
Publication year - 2014
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2014.2621.x
Subject(s) - neuroprotection , brimonidine , betaxolol , timolol , medicine , glaucoma , ophthalmology , agonist , pharmacology , neuroscience , anesthesia , biology , receptor
Glaucoma causes vision loss through the degeneration of retinal ganglion cells and their axons. Lowering IOP does not necessarily stop degeneration. Therefore neuroprotection is directed at neurons independently of its effects on IOP [1]. As the topical ocular hypotensive treatment is the main option in glaucoma nowadays, the direct neuroprotective effect of hypotensive eye drops is important. It has been postulated that PG analogues may have an IOP independent neuroprotective effect at clinically available intracameral concentration [2]. In vivo experiments demonstrated the neuroprotective properties of betaxolol [3]. The recent study of LoGTS demonstrates that the α2 agonist brimonidine may have a beneficial effect on visual function independent of IOP lowering [4]. Our recent research revealed the high antioxidant activity of fixed combinations of carboanhydrase inhibitors with timolol [5]. References 1. Cheung W, Guo L, Cordeiro MF. Optom Vis Sci. 2008;85:406‐416. 2. Yamagishi R., et al. Exp. Eye Res. 2011;93:265‐270. 3.Osborne NN, et al. Brain Res. 1997;751:113–123. 4.Krupin T, et al. 2011;151(4):671– 681. 5.Kurysheva N.I., et al. Rus. Ophthalm. J. 2013;6(2):41 – 45.