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Genetic Control of Complement Activation in Humans and Age Related Macular Degeneration

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Inflammation and Retinal Disease: Complement Biology and Pathology

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 703))

Abstract

The major focus of our research is to understand how age-related macular degeneration (AMD) develops. It is known that genetic variation can explain much of the risk of developing AMD. However, we do not know what controls the transition between a normal fundus and the extensive accumulation of subretinal inflammatory material that we recognize as drusen in AMD. We do know that the accumulation of this inflammatory material that characterizes the maculopathy underlying AMD is by far the most important predictor of late AMD. Late or advanced forms of AMD include geographic atrophy in which there is patchy death of the retina and exudation in which abnormal neovascularization invades the subretinal or subretinal pigment epithelial space. Thus, preventing the accumulation of the inflammatory debris underneath the retina could be expected to alleviate much of the vision loss from this devastating disease.

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Acknowledgements

Supported in part by NIH grant EY 014467, the Foundation Fighting Blindness, Owing Mills, MD; the American Health Assistance Foundation, Clarksburg, MD; and the Max Kade Foundation, Inc, New York, NY.

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Correspondence to Laura A. Hecker .

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Hecker, L.A., Edwards, A.O. (2010). Genetic Control of Complement Activation in Humans and Age Related Macular Degeneration. In: Lambris, J., Adamis, A. (eds) Inflammation and Retinal Disease: Complement Biology and Pathology. Advances in Experimental Medicine and Biology, vol 703. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-5635-4_4

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