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Hyperactive immune resistance brings blindness in old age
Date:7/24/2008

Age-dependent macular degeneration (AMD) is the commonest cause of blindness in the western industrialised nations. Hereditary changes in the regulation of the immune system influence the risk of contracting AMD. Opthalmologists at the University Clinic in Bonn, working in co-operation with researchers from Gttingen, Regensburg and Great Britain, have now, for the first time, demonstrated that in cases of senile blindness the patients immune resistance is hyperactive throughout his entire body.

An Anglo-German research team embracing immunologists from Gttingen University has added a further important aspect to our current knowledge of the processes leading to senile blindness. For the first time, they have been able to show that in the case of patients with AMD their entire immune system is hyperactive. It had not previously been known whether such an immune reaction affecting the entire body played any role in this eye disease.

The investigation was conducted by scientists from Bonn, Gttingen, Regensburg and Oxford under the leadership of Privatdozent Dr. Hendrik Scholl of Bonn Universitys Eye Clinic. The results achieved by this research team have now been published in the current edition of the PLoS ONE: http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002593

Faults in the (immune) System

The Anglo-German research team worked on the hypothesis that one cause of the appearance of senile blindness, AMD, might be faulty regulation of the so-called complement system. This system is an important element in our hereditary immune resistance, and is involved where inflammatory reactions occur. Previously, it had only been known that changes in genes containing the hereditary information for proteins in the complement system increase the risk of contracting AMD. Some of these proteins activate, others inhibit, the comp
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Contact: Dr. Hendrik Scholl
hendrik.scholl@ukb.uni-bonn.de
49-228-287-15505
University of Bonn
Source:Eurekalert

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