gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

What is the orign of AMD: new pathogenetical concepts

Meeting Abstract

Suche in Medline nach

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogSA.07.01

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dog2004/04dog343.shtml

Veröffentlicht: 22. September 2004

© 2004 Pauleikhoff.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

In this minisymposium on AMD the different aspects of macular aging and AMD will be explained in detail. In this short overview the different important steps in the pathogenesis of AMD will be highlighted.

Because of the lifelong light exposure of the central retina oxidative damage is present in the outer retina. Especially the photoreceptor outer segments are vulnerable bercause of their extremly high concentrations of unsaturated fatty acids. Oxidatively damaged molecules are phagicytized by the RPE. This material will be vdegraded in the RPE lysosomes, but because of maldigestion lipid and protein molecules accumulated in these organs resulting in lipofuszin granula. This accumulation can exaggerate to such an extend, that in the RPE cells apoptotic cell death will be induced resulting in geographic atrophy. In addition material will be exported by the RPE in the direction of the choroid. This results in an accumulation of debris in the underlaying Bruch´s Membrane. Due to changes in this structure the complement system will be activated. Their cytotoxic end products may attact the RPE, but these cells produce as a defense mechanism extensively extracellular matrix proteins to antagonize the attacing complement proteins. The accumulation of this material results in drusen and diffuse deposits in BM. In addition the activation of complement proteins may also result in changes of growth factors concentrations wich induces angiogenesis in the choriocapillaris resulting in choroidal neovascularisation.

In the following presentations the different steps of this complex aging process of the retina will be demonstrated in detail and possible treeatment options will be discussed.