Dipender Gill

The paper identifies 57 druggable targets for MASLD using genetic data and evaluates their therapeutic potential through Mendelian randomization and structural modeling.

This paper investigates the causal impact of opioid use disorder on brain health outcomes using observational and genetic analyses, finding increased dementia risk associated with both OUD diagnoses and genetic predisposition to OUD.

This paper introduces MrDAG, a Bayesian Mendelian randomization method that models complex dependencies among multiple exposures and outcomes to improve causal effect estimation, highlighting education and smoking as key interventions for mental health.

This paper introduces Multi-response Mendelian randomization (MR2) to identify shared and distinct exposures for multiple disease outcomes, showing improved power and accuracy by accounting for residual correlations between outcomes.

TwoStepCisMR provides a method and R package to reduce bias in cis-Mendelian randomisation by addressing confounding through linkage disequilibrium.

This study conducts a trans-ancestry GWAS using chronic ALT elevation as a proxy for NAFLD, identifies 77 significant loci, and validates 17 SNPs with histology and imaging data, revealing genetic links to metabolic and inflammatory traits.

This study identifies 144 genetic loci associated with abdominal aortic aneurysm and highlights PCSK9 as a therapeutic target through Mendelian Randomization and pre-clinical validation.

The paper clusters genetic variants associated with body mass index to identify distinct biological mechanisms underlying obesity and its impact on coronary heart disease.

This study examines how educational attainment modifies polygenic scores for cardiovascular risk factors using UK Biobank data, finding mixed effects across traits.

This study evaluates if African American or multi-ethnic polygenic risk scores improve type 2 diabetes prediction in continental Africans, finding that African American-derived scores are more predictive.

This study uses Mendelian randomization to show that genetically proxied IL-6 signaling inhibition reduces COVID-19 risk but increases pneumonia risk.

This study uses Mendelian randomization to examine if ACE inhibitors or cardiometabolic risk factors affect lung ACE2 and TMPRSS2 expression or plasma ACE2 levels, finding no overall association.

This paper conducts a genome-wide association study (GWAS) of skin and soft tissue infections (SSTIs), identifies genetic loci, and shows that BMI and smoking increase SSTI risk.

The paper uses genetic variants to investigate side effects and repurposing potential of antihypertensive drugs, finding a link between calcium channel blockers and increased diverticulosis risk.