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Abstract #20099 Published in IGR 9-4
Distribution of amyloid precursor protein and amyloid-β immunoreactivity in DBA/2J glaucomatous mouse retinas
Goldblum D; Kipfer-Kauer A; Sarra GM; Wolf S; Frueh BEInvestigative Ophthalmology and Visual Science 2007; 48: 5085-5090
PURPOSE: Evidence suggests that altered metabolism of amyloid precursor protein (APP) may play a role in the pathophysiology of retinal ganglion cell (RGC) death in the etiology of glaucoma. The authors sought to determine the distribution of APP and amyloid-β (A-β) in DBA/2J glaucomatous mouse retinas. METHODS: The retinas of three- and 15-month-old DBA/2J mice and C57/BL-6 mice (control group) were fixed with 4% paraformaldehyde and processed for immunohistochemistry. Antibodies used included a polyclonal antibody to the C terminus of A-β 40 and a polyclonal antibody to the APP ectodomain. Immunohistochemically stained tissue was graded using light microscopy. Distribution and semiquantitative expression of APP and A-β in young and old glaucomatous and normal retinas were determined and compared. RESULTS: Strong APP and A-β immunoreactivity was found in the RGC layer, optic nerve, and pia/dura of old DBA/2J retinas, with considerably higher intensity found in the old compared with the young DBA/2J mice. In contrast to glaucomatous mice, the control group did not show any notable age-related difference. CONCLUSIONS: Disruption of the homeostatic properties of secreted APP with consecutive A-β cytotoxicity might be a contributing factor of ganglion cell loss in glaucomatous mouse retinas.
Dr. D. Goldblum, Department of Ophthalmology, Inselspital, University of Bern, Switzerland. dgoldblum@uhbs.ch
Classification:
2.13 Retina and retinal nerve fibre layer (Part of: 2 Anatomical structures in glaucoma)
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
3.3 Immunohistochemistry (Part of: 3 Laboratory methods)
