Gibran Hemani

This study evaluates the causal relationship between DNA methylation and CRP using Mendelian randomization and finds potential causal effects of DNA methylation on CRP levels at three CpG sites.

PhenoSpD estimates phenotypic correlations and corrects multiple testing using GWAS summary statistics, reducing dimensionality for complex traits.

The paper investigates genetic overlap between non-syndromic cleft lip/palate and facial morphology using polygenic risk scores and Mendelian randomization, finding a causal relationship with philtrum width.

This study identifies 139 common and 4 rare genetic variants associated with type 2 diabetes through GWAS and integrates gene expression and epigenomic data to highlight potential functional genes and regulatory mechanisms.

The paper investigates whether DNA methylation mediates genetic risk for type 1 diabetes by analyzing SNP-methylation associations across different life stages.

Meffil normalizes and analyzes large DNA methylation datasets, reducing memory usage and technical variation while improving EWAS power.

This study uses Mendelian randomization to identify genetic loci that may influence disease through DNA methylation changes, finding 1,191 effects across 62 traits with high replication in UK Biobank.

The paper identifies gene targets for brain-related traits using transcriptomic and methylomic data from blood, finding strong correlations between genetic effects in brain and blood tissues.

The paper introduces an extended Mendelian randomisation method to infer causal directions between traits, showing DNA methylation is more likely causal but sensitive to measurement error.

The paper develops a method to partition phenotypic variance attributable to parent-of-origin effects using genomic relatedness matrices.

LD Hub provides a centralized database and web interface for performing LD score regression on GWAS summary data to estimate SNP heritability and genetic correlations across traits.