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Human Molecular Genetics Advance Access originally published online on September 20, 2005
Human Molecular Genetics 2005 14(21):3227-3236; doi:10.1093/hmg/ddi353
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© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Hypothetical LOC387715 is a second major susceptibility gene for age-related macular degeneration, contributing independently of complement factor H to disease risk

Andrea Rivera1,{dagger}, Sheila A. Fisher2,{dagger}, Lars G. Fritsche1, Claudia N. Keilhauer3, Peter Lichtner4,5, Thomas Meitinger4,5 and Bernhard H.F. Weber1,*

1Institute of Human Genetics, University of Regensburg, Franz-Josef-Strauss-Allee 11, D-93053 Regensburg, Germany, 2Department of Medical and Molecular Genetics, Guy's King's and St Thomas' School of Medicine, King's College London, UK, 3Department of Ophthalmology, University Eye Clinic, Wuerzburg, Germany, 4Institute of Human Genetics, Technical University Munich, D-81675 Munich, Germany and 5Institute of Human Genetics, GSF National Research Centre for Environment and Health, D-85764 Neuherberg, Germany

* To whom correspondence should be addressed. Tel: +49 9419445400; Fax: +49 9419445401; Email: bweb{at}biozentrum.uni-wuerzburg.de

Received August 23, 2005; Accepted September 16, 2005

Age-related macular degeneration (AMD) is a multifactorial disease and a prevalent cause of visual impairment in developed countries. Risk factors include environmental components and genetic determinants. The complement factor H (CFH) has been the first major susceptibility gene for AMD identified within 1q32. Here, we focused on a second region of interest in 10q26 where a recent meta-analysis revealed strongest evidence for linkage to AMD at a genome-wide significance level. Within an interval of 22 Mb, we have analyzed 93 single nucleotide polymorphisms for allelic association with AMD in two independent case–control cohorts of German origin (AMDcombined n=1166; controlscombined n=945). Significant association was found across a 60 kb region of high linkage disequilibrium harboring two genes PLEKHA1 and hypothetical LOC387715. The strongest association (P=10–34) centered over a frequent coding polymorphism, Ala69Ser, at LOC387715, strongly implicating this gene in the pathogenesis of AMD. Besides abundant expression in placenta, we demonstrate weak expression of LOC387715 in the human retina. At present, however, there is no functional information on this gene, which appears to have evolved recently within the primate lineage. The joint contribution of the common risk allele at LOC387715, Ala69Ser, and at CFH, Tyr402His, was assessed in our case–control population, which suggests an additive model indicating an independent contribution of the two gene loci to disease risk. Our data show a disease odds ratio of 57.6 (95% CI: 37.2, 89.0) conferred by homozygosity for risk alleles at both CFH and LOC387715 when compared with the baseline non-risk genotype.

{dagger} The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.


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