Ville Karhunen

This study uses Mendelian randomization to investigate ECS gene variants and their associations with dementia risk and biomarkers, finding some links but no strong causal evidence.

This paper identifies shared genetic loci between inflammation and cancer risk using non-causal associations, revealing potential therapeutic targets.

The paper conducts a multi-ancestry, trans-generational GWAS meta-analysis of gestational diabetes and glycemic traits, identifying novel loci and highlighting limited pregnancy-specific genetic effects.

This study uses genetic data to show that HMGCR inhibition affects coronary artery disease and type 2 diabetes through different causal pathways, with BMI and LDL-C playing distinct roles.

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 FiniMOM, a Bayesian fine-mapping method that improves detection of multiple causal variants using non-local priors and summary data from GWAS.

This study conducts a genome-wide association meta-analysis of childhood aggression across multiple raters, instruments, and ages, identifying genetic correlations with various traits but no genome-wide significant SNPs.

This study investigates how polygenic scores and environmental factors jointly predict educational achievement, finding significant gene-environment correlation but no overall gene-environment interaction.

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.

GWAS in over one million individuals identify 611 loci across risk tolerance and risky behaviors, revealing shared genetic architecture and implicating glutamatergic and GABAergic neurotransmission.

This study applies polygenic risk scores to a single cohort to identify shared genetic aetiology across hundreds of traits, revealing pleiotropy and novel genetic associations.

This study investigates the genetic contributions to gestational weight gain, finding that maternal common variants explain about 20% of variability, while fetal variants have a minor role.

The paper identifies genetic variants associated with post-term birth in Northern Finland cohorts and links some to gene expression changes.

This study identifies genetic loci associated with early childhood growth phenotypes and links them to later adiposity traits, suggesting potential targets for obesity prevention.