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27 November 2006

Why the Retina Gets Smothered in Metabolic Waste

Heidelberg scientist distinguished by the "Großloge der Deutschen Odd Fellows" for pioneering work on the causes of age-related macular degeneration

Why do the photoreceptors of the retina fail to function when the eye is affected by a widespread age-related disorder known as macular degeneration? Dr. Marion Bergmann of the Applied Tumour Biology Department of Heidelberg University's Institute of Pathology has detected a molecular mechanism causing the congestion of the cells with waste products.

For this pioneering study the 37-year-old biologist, a member of the research group headed by Professor Dr. Jürgen Kopitz, has been awarded the research prize of the "Großloge der Deutschen Odd Fellows", worth 5,000 euros. The study has been published in the Journal of the Federation of American Societies for Experimental Biology.

Age-related macular degeneration (AMD) is a disorder notably affecting older people and leading to severe visual impairment and blindness. In Germany two to three million people suffer from this condition. Their sight is impaired by the failure of the macula, a small spot near the centre of the retina, where under normal circumstances vision is especially sharp.

In a healthy retina the photosensitive cells renew themselves constantly. Cellular waste is degraded by enzymes in the pigment epithelium, the layer immediately below the photoreceptors that nourishes the retinal cells. This work is done in the tiny digestive organelles called lysosomes. The function of these lysosomes decreases with age.

How does toxic "metabolic waste" exacerbate the decline of photoreceptors?

So far, little is known about the causes for the failure of these organelles. Bergmann and her research group investigated the effects of lipofuscin on the function of the digestive organelles. Lipofuscin is an aging pigment left over after the breakdown of damaged blood cells. This toxic "metabolic waste" is deposited not only in the retina but also in heart muscle cells or the liver.

In her research Bergmann concentrated on the lipofuscin fluorophore "A2-E". Experiments showed that too much A2-E inhibits the so-called proton pump, small channels in lysosome membrane maintaining the acidic intralysosome pH. If these channels are "blocked", intralysosome pH increases, thus sabotaging the digestive function of the organelles. In this way, lipofuscin deposits interfere with normal waste disposal in the photoreceptors and possibly promote the degeneration of the macula.

Humanitarian society provides funding for research

The Research Prize for the Prevention of Age-Related Macular Degeneration (5,000 euros) was presented for the first time in 2006 and in future is to be awarded every two years. It is donated by the "Großloge der Deutschen Odd Fellows", a charitable organisation established in the late 19th century and originating in Baltimore (USA).

Literature
M. Bergmann, F. Schütt, F.G. Holz, J. Kopitz: Inhibition of the ATP-driven photon pump in RPE lysosomes by the major lipofuscin fluorophore A2-E may contribute to the pathogenesis of age-related macular degeneration. FASEB Journal 2004 Mar; 18(3):562-4. Epub 2004 Jan 8. PMID:14715704

The original article can be requested from the Press Dept. of Heidelberg University Hospital: contact@med.uni-heidelberg.de

Please address any inquiries to:
Dr. Marion Bergmann
Applied Tumour Biology Dept.
Institute of Pathology
Heidelberg University Hospital
Im Neuenheimer Feld 220/221
D-69120 Heidelberg
e-mail: marion.bergmann@med.uni-heidelberg.de

Inquiries from journalists should be addressed to
Dr. Annette Tuffs
Press and Public Relations Officer
Heidelberg University Hospital
Medical Faculty of the University of Heidelberg
Im Neuenheimer Feld 672
phone: 06221/564536
fax: 06221/564544
mobile: 0170/5724725
e-mail : Annette_Tuffs@med.uni-heidelberg.de
www.klinikum.uni-heidelberg.de

Dr. Michael Schwarz
Press Officer of the University of Heidelberg
phone: 06221/542310, fax: 54317
michael.schwarz@rektorat.uni-heidelberg.de
http://www.uni-heidelberg.de/presse/index.html


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