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1 General aspects (0)   1.1 Epidemiology (2)   1.2 Population genetics (5)   1.3 Pathogenesis (5)   1.4 Quality of life (2)   1.5 Glaucomas as cause of blindness (3)   1.6 Prevention and screening (3) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (2)   2.2 Cornea (6)   2.3 Sclera (1)   2.4 Anterior chamber angle (0)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (7)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (1)     2.6.1 Production (1)     2.6.2 Outflow (3)       2.6.2.1 Trabecular meshwork (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (9)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (1)   2.9 Ciliary body (2)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (3)   2.13 Retina and retinal nerve fibre layer (21)   2.14 Optic disc (17)   2.15 Optic nerve (3)   2.16 Chiasma and retrochiasmal central nervous system (0)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (0)   3.2 Electron microscopy (1)   3.3 Immunohistochemistry (14)   3.4 Molecular genetics (4)     3.4.1 Linkage studies (15)     3.4.2 Gene studies (1)   3.5 Molecular biology incl. 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with intraocular tumors (0)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (0)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (0)       9.4.11.2 Glaucomas in aphakia and pseudophakia (1)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (0)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (1)     9.4.15 Glaucoma in relation to systemic disease (12)     9.4.20 Other (1) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (7) 11 Medical treatment (0)   11.1 General management, indication (10)   11.2 Cholinergic drugs (0)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (8)     11.3.4 Betablocker (14)     11.3.5 Other (0)   11.4 Prostaglandins (23)   11.5 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Without tube implant (4)     12.8.2 With tube implant or other drainage devices (7)     12.8.3 Non-perforating (12)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (13)     12.8.11 Complications, endophthalmitis (8)   12.9 Trabeculotomy, goniotomy (0)   12.10 Cyclodestruction (5)   12.11 Cyclodialysis (3)   12.12 Cataract extraction (1)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (2)   12.14 Combined cataract extraction and glaucoma surgery (3)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (5)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (2)   12.20 Other (2) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (0) 15 Miscellaneous (1)

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Abstract #10499 Published in IGR 6-1

Retinal neurodegeneration in the DBA/2J mouse: a model for ocular hypertension

Schuettauf F; Rejdak R; Walski M; Frontczak Baniewicz M; Voelker M; Blatsios G; Shinoda K; Zagorski Z; Zrenner E; Grieb P
Acta Neuropathologica 2004; 107: 352-358

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Mice of the DBA/2J strain spontaneously develop complex ocular abnormalities, including glaucomatous loss of retinal ganglion cells (RGC). In the present study, the ultrastructural features of retinal neurodegeneration in DBA/2J mice of various ages (three, six, eight and 11 months) are described. By three months, RGC apoptosis characterized by electron-dense karioplasm and cytoplasm of ganglion cells was observed. The occurrence of apoptotic ganglion cells peaked at the age of six months. Above this age, necrosis characterized by swelling and electron-rare cytoplasm appeared to be the prevailing form of cell death. Mueller glia activation increased with age, but there were no signs of leukocyte infiltration. At eight and 11 months, signs of neoangiogenesis were found both at the ultrastructural level and during clinical examinations. In these older animals, myelin-like bodies, most probably representing the intracellular aggregates of phospholipids in irreversibly injured cells, were also seen. Photoreceptor cells were not affected at any age. These observations suggest that retinal degeneration in the DBA/2J mice does not involve recruitment of bloodborne inflammatory/phagocytozing cells, and that apoptosis is gradually replaced by necrosis as the predominant pathway of RGC death. Retinal degeneration in three- to 11-month-old DBA/2J mice partially resembles human pigment dispersion syndrome and pigmentary glaucoma with characteristic anterior segment changes and elevation of intraocular pressure. However, neovasculogenesis and myelin-like bodies are observed during aging. Therefore, the DBA/2J model requires judicious interpretation as a glaucoma model.

Dr. F. Schuettauf, Department of Experimental Ophthalmology, University Eye Hospital, Roentgenweg 11, 72076 Tuebingen, Germany

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Classification:

5 Experimental glaucoma; animal models

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