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1 General aspects (0)   1.1 Epidemiology (8)   1.2 Population genetics (0)   1.3 Pathogenesis (4)   1.4 Quality of life (13)   1.5 Glaucomas as cause of blindness (5)   1.6 Prevention and screening (11) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (12)   2.2 Cornea (28)   2.3 Sclera (9)   2.4 Anterior chamber angle (8)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (9)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (1)     2.6.2 Outflow (2)       2.6.2.1 Trabecular meshwork (4)       2.6.2.2 Uveoscleral (1)     2.6.3 Compostion (2)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (2)   2.9 Ciliary body (1)   2.10 Lens (1)   2.11 Vitreous body (1)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (11)   2.13 Retina and retinal nerve fibre layer (30)   2.14 Optic disc (28)   2.15 Optic nerve (3)   2.16 Chiasma and retrochiasmal central nervous system (11)   2.17 Stem cells (1)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (4)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (1)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (1)     3.4.2 Gene studies (27)   3.5 Molecular biology incl. 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pharmacoeconomics (6) 15 Miscellaneous (20)

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Abstract #60976 Published in IGR 17-1

Recent Developments in Understanding the Role of Aqueous Humor Outflow in Normal and Primary Open Angle Glaucoma

Hann CR; Fautsch MP
Current ophthalmology reports 2015; 3: 67-73

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Primary open angle glaucoma (POAG) is the second leading cause of blindness in the world's rapidly aging population. POAG is characterized by progressive degeneration of neural structures in the posterior segment, often associated with a concomitant elevation of intraocular pressure. Changes in IOP are believed to be caused by a disruption in the normal outflow of aqueous humor. This article reviews recent research associated with normal and POAG aqueous humor outflow. Novel findings elucidating biochemical and pathological changes in the ocular tissues affected in POAG are presented. Stem cell research, identification of lymphatic markers, and increased use of mouse models give researchers exciting new tools to understand aqueous humor outflow, changes associated with POAG and identify underlying causes of the disease.

Department of Ophthalmology Mayo Clinic 200 First Street SW Rochester, MN 55905 USA hann.cheryl@mayo.edu.

Full article

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Classification:

2.6.2 Outflow (Part of: 2 Anatomical structures in glaucoma > 2.6 Aqueous humor dynamics)

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