Zusammenfassung
Nach Schätzung der WHO sind etwa 105 Millionen Menschen weltweit vom Glaukom betroffen. Das Glaukom kann als progressive Optikoneuropathie mit struktureller Schädigung des Sehnervenkopfs und Untergang retinaler Ganglienzellen definiert werden. Obwohl ein erhöhter IOD für das Glaukom als ursächlich gilt, führt eine Drucksenkung häufig nicht zur Besserung. Aus diesem Grund werden noch andere ätiologische Faktoren vermutet. Diese sollen im folgenden Beitrag aufgezeigt und die Rolle von Neuroprotektiva bei Glaukom diskutiert werden. Das für das Glaukom spezifische Muster des Ganglienzelluntergangs lässt vermuten, dass bestimmte Ganglienzellen empfindlicher sein könnten als andere. Die Theorie des „kumulativen Schadens“ beinhaltet hier die Hypothese, dass der verzögerte Beginn vieler neurodegenerativer Erkrankungen, wie Glaukom, M. Alzheimer oder M. Parkinson, auf die altersabhängige Kumulation toxischer Substanzen in den Ganglienzellen zurückzuführen ist. Dahingegen beruht die Theorie der „singulären Schädigung“ auf der Vermutung, dass sich bestimmte Ganglienzellen durch die Expression sogenannter „Mutant-response“-Gene in einem Zustand reduzierter Homöostase befinden. Überlegenswerte Therapieansätze, die hinsichtlich ihres Nebenwirkungsprofils und ihrer Wirksamkeit im Tierversuch in Frage kommen, werden dargestellt.
Abstract
According to estimates made by WHO, approximately 105 million people are affected worldwide by glaucoma. This can be defined as progressive optic neuropathy with structural damage of the optic nerve head and death of retinal ganglion cells. Although elevated IOP is considered responsible for glaucoma, lowering the pressure often does not result in improvement. For this reason, other etiological factors are presumed, which are presented in the following contribution. The role of neuroprotective agents in the treatment of glaucoma is discussed. The pattern of ganglion cell death specific to glaucoma seems to suggest that certain ganglion cells could be more sensitive than others. The theory of “cumulative damage” in this case includes the hypothesis that the delayed onset of many neurodegenerative diseases such as glaucoma, Alzheimer’s disease, or Parkinson’s disease can be attributed to the age-related accumulation of toxic substances in the ganglion cells. On the contrary, the theory of “singular damage” is based on the assumption that certain ganglion cells are in a state of reduced homeostasis caused by the expression of so-called mutant response genes. Therapeutic approaches worthy of consideration based on their side effect profile and efficacy in animal trials, are presented.
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Osborne, N.N., Schmidt, KG. Neuroprotektion bei Glaukom bleibt ein Konzept. Ophthalmologe 101, 1087–1092 (2004). https://doi.org/10.1007/s00347-004-1129-7
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DOI: https://doi.org/10.1007/s00347-004-1129-7
Schlüsselwörter
- Chronisches Offenwinkelglaukom
- Neuroprotektiva
- Ganglienzelltod
- Neurodegenerative Erkrankungen
- Gesichtsfeldverfall
- Nebenwirkungsprofil