作者
Gareth J McKay, Chris C Patterson, Usha Chakravarthy, Shilpa Dasari, Caroline C Klaver, Johannes R Vingerling, Lintje Ho, Paulus TVM de Jong, Astrid E Fletcher, Ian S Young, Johan H Seland, Mati Rahu, Gisele Soubrane, Laura Tomazzoli, Fotis Topouzis, Jesus Vioque, Aroon D Hingorani, Reecha Sofat, Michael Dean, Julie Sawitzke, Johanna M Seddon, Inga Peter, Andrew R Webster, Anthony T Moore, John RW Yates, Valentina Cipriani, Lars G Fritsche, Bernhard HF Weber, Claudia N Keilhauer, Andrew J Lotery, Sarah Ennis, Michael L Klein, Peter J Francis, Dwight Stambolian, Anton Orlin, Michael B Gorin, Daniel E Weeks, Chia‐Ling Kuo, Anand Swaroop, Mohammad Othman, Atsuhiro Kanda, Wei Chen, Goncalo R Abecasis, Alan F Wright, Caroline Hayward, Paul N Baird, Robyn H Guymer, John Attia, Ammarin Thakkinstian, Giuliana Silvestri
发表日期
2011/12
期刊
Human mutation
卷号
32
期号
12
页码范围
1407-1416
出版商
Wiley Subscription Services, Inc., A Wiley Company
简介
Age‐related macular degeneration (AMD) is the most common cause of incurable visual impairment in high‐income countries. Previous studies report inconsistent associations between AMD and apolipoprotein E (APOE), a lipid transport protein involved in low‐density cholesterol modulation. Potential interaction between APOE and sex, and smoking status has been reported. We present a pooled analysis (n = 21,160) demonstrating associations between late AMD and APOε4 (odds ratio [OR] = 0.72 per haplotype; confidence interval [CI]: 0.65–0.74; P = 4.41×10−11) and APOε2 (OR = 1.83 for homozygote carriers; CI: 1.04–3.23; P = 0.04), following adjustment for age group and sex within each study and smoking status. No evidence of interaction between APOE and sex or smoking was found. Ever smokers had significant increased risk relative to never smokers for both neovascular (OR = 1.54; CI: 1.38–1.72; P …
引用总数
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