Programm                 "Degeneration und Regeneration– Grundlagen, Diagnostik und Therapie"


Hotelbuchung
   Hotel Registration
Grußwort
   Welcome address
Beteiligte Gesellschaften
   Societies involved
DOG Information
   DOG Information
Eröffnung des Kongresses
   Opening Ceremony
Preise
   Awards
Ablauf der Tagung 2003
   General overview of congress
Lageplan der Räumlichkeiten
   Map of Congress Center
Wissenschaftliche Themen
   Scientific topics
Symposien
   Symposia
Wissenschaftliches Programm
   Scientific program
Posterpräsentationen
   Poster Presentation
Kurse
   Courses
Begleitende Veranstaltungen
   Accompanying program
Arbeitssitzungen
   Working sessions
Rahmenprogramm
   Social program
Allgemeine Informationen
   General Information
Autorenindex
   Index of Authors
Industrieaussteller
   Commercial exhibitors
Sponsoren
   Sponsors
Impressum



DOG Homepage


Abstract
Abstract

Animal models of neovascular AMD

Fauser S., Krohne T., Kociok N., Kirchhof B., Joussen A. M.
Universität zu Köln, Zentrum für Augenheilkunde, Abteilung für Netzhaut- und Glaskörperchirurgie (Köln)

The lack of adequate animal models is a major problem in investigating choroidal neovascularisation (CNV) in age-related macular degeneration (AMD). Nevertheless, several models represent certain aspects of the disease. Here, we review available models of AMD. In the best established model, CNV is induced by laser-induced rupture of Bruch's membrane. However, the CNV is accompanied by an unspecific, local inflammation. Another popular model is the RCS rat where shed outer segments of the photoreceptor cells accumulate in the subretinal space due to a mutation in the Mertk gene. Therefore, it is predominantly a model for retinitis pigmentosa.
Transgenic animal models are becoming more and more important and help to elucidate pathogenesis and therapeutic strategies. In future, more disease-specific models will be developed despite the fact that the complex pathomechanism will make it unlikely that one single model will represent all aspects of CNV.
For example, the increased expression of VEGF in photoreceptors of transgenic mice induces a neovascularisation only in the retina. The intact Bruch’s membrane seems to be a mechanical and biochemical barrier for VEGF from the retina into the choriod. Transgenic mice overexpressing VEGF in RPE cells show enlarged choroidal vessels but no CNV, perhaps because a second protagonist, Angiopoietin-2, is not present.


Zurück | Back