ArticleScientific reports2024
Genome wide association study and genomic risk prediction of age related macular degeneration in Israel.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Genetic determinants of age-related macular degeneration in Middle Eastern populations: a systematic review.Frontiers in genetics · 2026Pooled it
- From Genetic Diagnosis to Therapeutic Implementation in Retinal Diseases: Translational Advances and Persistent Bottlenecks.Biomedicines · 2026Review
- Distinct Genetic Profiles Associated With Subretinal Drusenoid Deposits and Cardiovascular Risk in Age-Related Macular Degeneration.Translational vision science & technology · 2026Article
- Diverse-Ancestry GWAS of Age-Related Macular Degeneration on 16,108 Examined Cases and 18,038 Controls.Investigative ophthalmology & visual science · 2025Article
- Markedly Lower Rates of Age-Related Macular Degeneration in Malta Compared to European Countries: Results from The Malta Eye Study, Indicating Possible Divergent Genetic Ancestry?Clinical ophthalmology (Auckland, N.Z.) · 2025Article
- Fundus Image Deep Learning Study to Explore the Association of Retinal Morphology with Age-Related Macular Degeneration Polygenic Risk Score.Biomedicines · 2024Article
- Genetic Risk and OCT-Based Phenotypic Associations in Age-Related Macular Degeneration.Ophthalmology scienceArticle
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15 authors.
Funding
Abstract
The risk of developing age-related macular degeneration (AMD) is influenced by genetic background. In 2016, the International AMD Genomics Consortium (IAMDGC) identified 52 risk variants in 34 loci, and a polygenic risk score (PRS) from these variants was associated with AMD. The Israeli population has a unique genetic composition: Ashkenazi Jewish (AJ), Jewish non-Ashkenazi, and Arab sub-populations. We aimed to perform a genome-wide association study (GWAS) for AMD in Israel, and to evaluate PRSs for AMD. Our discovery set recruited 403 AMD patients and 256 controls at Hadassah Medical Center. We genotyped individuals via custom exome chip. We imputed non-typed variants using cosmopolitan and AJ reference panels. We recruited additional 155 cases and 69 controls for validation. To evaluate predictive power of PRSs for AMD, we used IAMDGC summary-statistics excluding our study and developed PRSs via clumping/thresholding or LDpred2. In our discovery set, 31/34 loci reported by IAMDGC were AMD-associated (P < 0.05). Of those, all effects were directionally consistent with IAMDGC and 11 loci had a P-value under Bonferroni-corrected threshold (0.05/34 = 0.0015). At a 5 × 10
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