May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Examination of Genetic Variants in HTRA1 and LOC387715 Within the 10q26 Region in Age-Related Macular Degeneration
Author Affiliations & Notes
  • E. A. Postel
    Ophthalmology, Duke University Eye Center, Durham, North Carolina
  • P. Gallins
    Center for Human Genetics, Duke University, Durham, North Carolina
  • W. K. Scott
    Center for Human Genetics, Duke University, Durham, North Carolina
  • S. Schimdt
    Center for Human Genetics, Duke University, Durham, North Carolina
  • M. A. Hauser
    Center for Human Genetics, Duke University, Durham, North Carolina
  • J. L. Hainers
    Center for Human Genetic Research, Vanderbilt University, Memphis, Tennessee
  • M. A. Pericak-Vance
    Center for Human Genetics, Duke University, Durham, North Carolina
  • Footnotes
    Commercial Relationships E.A. Postel, None; P. Gallins, None; W.K. Scott, None; S. Schimdt, None; M.A. Hauser, None; J.L. Hainers, None; M.A. Pericak-Vance, None.
  • Footnotes
    Support NIH grants EY12118, EY015216
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 4624. doi:
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      E. A. Postel, P. Gallins, W. K. Scott, S. Schimdt, M. A. Hauser, J. L. Hainers, M. A. Pericak-Vance; Examination of Genetic Variants in HTRA1 and LOC387715 Within the 10q26 Region in Age-Related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4624.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose:: Age-related macular degeneration (AMD) is a common complex disorder that affects the central region of the retina and is the leading cause of legal blindness in Caucasian Americans aged >65 years. Along with the Y402H variant of the complement factor H gene (CFH) on chromosome 1q32, several other genetic variants within 10q26 have been identified as susceptibility loci for AMD. However, the exact susceptibility variant within 10q26 is currently unknown.

Methods:: We compared two previously proposed SNPs, rs10490924 in LOC387715 and rs11200638 in HTRA1 (r2=0.93), by performing an association analysis in two unrelated datasets, one case-control one family-based. The case-control dataset included 644 cases and 265 controls and was analyzed by logistic regression using an additive model with adjustment for age and sex. The family-based dataset included cases with at least one sampled relative (n = 205 families), and were analyzed for association using the APL (Association in the Presence of Linkage) statistic.

Results:: In the case-control dataset, both variants had strong association with AMD (P < 0.0001), with similar odds ratios (rs10490924: 2.13 (95% CI 1.65-2.75); rs11200638: 2.00 (95% CI 1.56-2.57)). Using only cases with neovascularization (n=405) and controls with no drusen (n=193), the results were similar but the odds ratios stronger (rs10490924: 2.98 (95% CI 2.14-4.16); rs11200638: 2.80 (95% CI 2.03-3.88)). These data suggest the risk may be stronger for neovascular AMD. The association results in the family-based dataset, although not as strong, confirmed these effects (rs11200638 (P = 0.02), rs10490924 (P = 0.05).

Conclusions:: These data do not allow us to differentiate between the potential roles of LOC387715 and HTRA1 in AMD.

Keywords: age-related macular degeneration • genetics 
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