{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T18:15:48Z","timestamp":1778782548505,"version":"3.51.4"},"reference-count":43,"publisher":"Public Library of Science (PLoS)","issue":"5","license":[{"start":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T00:00:00Z","timestamp":1778716800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:p>At present, the genetic architecture underlying traits linked to Age-related eye disease (ARED) remains largely unexplored. We utilized Genomic Structural Equation Modeling (Genomic-SEM) and various Post-processing analysis of Genome-Wide Association Studies (GWAS) to identify statistically prioritized candidate single nucleotide polymorphisms (SNPs) associated with independent ARED variants. A total of 11 genome-wide significant loci were identified in the study. By applying diverse transcriptome-wide association approaches, we analyzed tissue-, cell layer-, and genomic element-associated gene signals reflecting age-related ocular vulnerabilities, alongside their functional annotations in relation to ARED. 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