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The optic nerve is a bundle of fibers and axons projecting from specialized retinal neurons, the retinal ganglion cells (RGCs), which make synaptic connections to the visual cortex. Glaucoma is a chronic and progressive degenerative neuropathy of the optic nerve with death of RGCs, and is a leading cause of irreversible blindness. A risk factor for glaucoma is high intraocular pressure (IOP). However, the etiology of glaucoma is unknown and it is likely multifactorial, and upregulation of neurotoxic factors is implicated. Glaucoma can often be independent of high IOP (e.g., normal-tension glaucoma), and disease progression is independent of constant high IOP. Currently, the only pharmacological treatments approved for glaucoma are IOP-lowering drugs, which simply delay disease progression. Optic nerve neuropathy, thinning of the nerve fiber layer, degeneration of the axons, and eventual death of the RGCs continue. In the past decade, experimental therapeutic approaches have evolved to address the complex and multifactorial etiology of this disease. Two approaches are the rescue of RGCs from death by utilizing neuroprotection, and the prevention of RGC death by reducing neurotoxicity. This review draws attention to the potential of neuroprotection in glaucoma, specifically focusing on growth factors termed neurotrophins and their receptors. Copyright (copyright) 2011 Prous Science, S.A.U. or its licensors. All rights reserved.
H.U. Saragovi. McGill University, Department of Pharmacology and Therapeutics, Jewish General Hospital, 3755 Cote St. Catherine, E535, Montreal, QC H3T 1E2, Canada. Email: uri.saragovi@mcgill.ca
11.8 Neuroprotection (Part of: 11 Medical treatment)
11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)