ArticleOphthalmology and therapy2024
Evidence for Genetic Causal Relationships Between Multiple Immune-Mediated Inflammatory Diseases and Age-Related Macular Degeneration: A Univariable and Multivariable Mendelian Randomization Study.
Article in Ophthalmology and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Causal effects of antibody-mediated immunity to pathogens on five ophthalmic diseases: a Mendelian randomization study.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Cross-speciality collaborative care in complex immune-mediated inflammatory diseases: treating the person living with the condition.BMC medicine · 2025Review
- Identification of Biomarkers for Oxidative Stress in Age-Related Macular Degeneration: Combining Transcriptomics and Mendelian Randomization Analysis.Translational vision science & technology · 2025Article
- Does uveitis increase the risk of age-related wet macular degeneration? A Mendelian randomization study.International journal of ophthalmology · 2025Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
introductionWith the global aging population on the rise, age-related macular degeneration (AMD) poses a growing healthcare burden. Prior research hints at immune-mediated inflammatory diseases (IMIDs) potentially elevating AMD risk via diverse mechanisms. However, causality remains disputed as a result of confounding factors. Hence, our Mendelian randomization (MR) study aims to untangle this link, mitigating confounding effects to explore the IMID-AMD causal relationship. This study aims to investigate the causal relationship between IMIDs and AMD, providing new strategies for the prevention and treatment of AMD in clinical practice.
methodsThis study was registered with PROSPERO, CRD42023469815. We obtained data on IMIDs and AMD from Genome-Wide Association Studies (GWAS) summary statistics and the FinnGen consortium. Rigorous selection steps were applied to screen for eligible instrumental single nucleotide polymorphisms (SNPs). We conducted univariate Mendelian randomization, inverse variance-weighted (IVW), weighted median, Mendelian randomization-Egger (MR-Egger), and multivariate Mendelian randomization (MVMR) analyses. Various sensitivity analysis methods were employed to assess pleiotropy and heterogeneity. The aim was to explore the causal relationships between IMIDs and AMD.
resultsThe MR analysis revealed that Crohn's disease (CD) (IVW: odd ratios (OR) 1.05, 95% CI (confidence interval) 1.01-1.10, p = 0.007), rheumatoid arthritis (RA) (IVW: OR 1.09, 95% CI 1.04-1.15, p = 0.0001), and type 1 diabetes (T1D) (IVW: OR 1.05, 95% CI 1.02-1.09, p = 0.001) were correlated with an elevated risk of AMD, while multiple sclerosis (MS) (IVW: OR 2.78E-18, 95% CI 2.23E-31 to 3.48E-05, p = 0.008) appeared to be protective against AMD. These findings were supported by an array of MR analysis methodologies and the MVMR approach.
conclusionOur study results, based on MR, provide genetic evidence indicating a causal relationship between specific IMIDs and AMD. CD, RA, and T1D are factors increasing the risk of AMD, while MS may have a protective effect.
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