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Erschienen in: Graefe's Archive for Clinical and Experimental Ophthalmology 8/2004

01.08.2004 | Review

Keypathophysiologic pathways in age-related macular disease

verfasst von: Felix Roth, Almut Bindewald, Frank G. Holz

Erschienen in: Graefe's Archive for Clinical and Experimental Ophthalmology | Ausgabe 8/2004

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Abstract

Purpose

To review current knowledge of key pathogenetic pathways in age-related macular disease (AMD).

Methods

Experimental evidence and clinical observations are reviewed.

Results

A number of common downstream pathophysiologic pathways appear to be relevant in AMD manifestations irrespective of primary heterogeneous etiologies. These include sequelae of oxidative damage, retinal pigment epithelium (RPE) cell dysfunction with accumulation of lipofuscin and impairment of lysosomal functions, deposition of subsequently incompletely degraded material at the basal RPE cell side and alterations in Bruch’s membrane extracellular matrix, immunologic responses to extracellular material (drusen) with subsequent growth of drusen, induction of choroidal neovascularization as a result of imbalance between anti-angiogenetic and proangiogenetic factors as well as cell death (geographic atrophy) without prior neovascular events.

Conclusions

Understanding is expanding regarding the sequence of events that lead to early and late lesions in AMD. Therapeutic approaches that focus on the molecular mechanisms are more likely to succeed than currently available treatment options as exemplified by the management of choroidal neovascularisations.
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Metadaten
Titel
Keypathophysiologic pathways in age-related macular disease
verfasst von
Felix Roth
Almut Bindewald
Frank G. Holz
Publikationsdatum
01.08.2004
Erschienen in
Graefe's Archive for Clinical and Experimental Ophthalmology / Ausgabe 8/2004
Print ISSN: 0721-832X
Elektronische ISSN: 1435-702X
DOI
https://doi.org/10.1007/s00417-004-0976-x

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