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1 General aspects (0)   1.1 Epidemiology (10)   1.2 Population genetics (0)   1.3 Pathogenesis (14)   1.4 Quality of life (14)   1.5 Glaucomas as cause of blindness (4)   1.6 Prevention and screening (8) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (5)   2.2 Cornea (22)   2.3 Sclera (6)   2.4 Anterior chamber angle (6)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (10)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (2)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (4)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (4)   2.9 Ciliary body (1)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (6)   2.13 Retina and retinal nerve fibre layer (14)   2.14 Optic disc (11)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (4)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (4)   3.2 Electron microscopy (1)   3.3 Immunohistochemistry (0)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (2)     3.4.2 Gene studies (38)   3.5 Molecular biology incl. 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associated with intraocular tumors (6)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (1)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (1)       9.4.11.2 Glaucomas in aphakia and pseudophakia (8)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (3)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (0)     9.4.15 Glaucoma in relation to systemic disease (22)     9.4.20 Other (1) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (4) 11 Medical treatment (0)   11.1 General management, indication (2)   11.2 Cholinergic drugs (2)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (1)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (0)     11.3.4 Betablocker (3)     11.3.5 Other (0)   11.4 Prostaglandins 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Miscellaneous (14)

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Abstract #51308 Published in IGR 14-3

Maintenance of retinal ganglion cell mitochondrial functions as a neuroprotective strategy in glaucoma

Osborne NN; del Olmo-Aguado S
Current opinion in pharmacology 2013; 13: 16-22

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Loss of vision in glaucoma occurs because retinal ganglion cells (RGCs) die. RGCs have probably more mitochondria than any other neurone in the CNS. It is proposed that stress to mitochondria of individual RGCs is a major trigger of the disease and also provides an explanation why different RGCs die at different times. Pharmacological agents that can maintain mitochondrial functions, in particular to attenuate oxidative stress and to sustain energy production, might therefore provide a novel way of slowing down RGC death and help in the treatment of glaucoma.

Fundación de Investigación Oftalmológica, Avda. Doctores Fernández-Vega 34, E-33012 Oviedo, Asturias, Spain. Electronic address: Neville.osborne@eye.ox.ac.uk.

Full article

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Classification:

3.6 Cellular biology (Part of: 3 Laboratory methods)
3.8 Pharmacology (Part of: 3 Laboratory methods)
2.13 Retina and retinal nerve fibre layer (Part of: 2 Anatomical structures in glaucoma)

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