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

被引:10
|
作者
Hecker, Laura A. [1 ]
Edwards, Albert O. [2 ]
机构
[1] Mayo Clin, Rochester, MN 55905 USA
[2] Univ Oregon, Inst Mol Biol, Eugene, OR 97403 USA
来源
INFLAMMATION AND RETINAL DISEASE: COMPLEMENT BIOLOGY AND PATHOLOGY | 2010年 / 703卷
关键词
FACTOR-H POLYMORPHISM; ALTERNATIVE PATHWAY; STARGARDT-DISEASE; FACTOR-B; VARIANT; RISK; SUSCEPTIBILITY; ASSOCIATION; ALLELES; ARMS2;
D O I
10.1007/978-1-4419-5635-4_4
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:49 / 62
页数:14
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