Venexia M. Walker

This study uses Mendelian randomization to identify risk factors for kidney function decline in CKD and the general population, finding causal effects of type-2 diabetes and high TSH.

The paper identifies age-dependent methylation quantitative trait loci (longitudinal mQTLs) across the lifespan using blood DNAm data from two cohorts, finding consistent genotype-by-age effects and associations with multiple phenotypes.

This study uses Mendelian randomization to assess how cardiometabolic drugs affect kidney function, finding specific drug targets influence eGFR and related biomarkers.

This paper uses Mendelian randomization to assess if existing drugs targeting lipid-lowering, anti-hypertensive, or anti-inflammatory pathways affect vascular dementia risk, finding potential benefits for beta-1 adrenergic receptor antagonists and risks for ACE inhibitors.

This paper develops a genetically informed drug-repurposing pipeline for diabetes using EHRs and validates two anti-hypertensive classes as glycemic regulators.

This paper reviews statistical methods to detect and adjust for collider bias in genetic and Mendelian randomization studies of disease progression using individual and summary-level data.

This study shows genetic associations of CRP variants with BMI differ between individuals with and without cardiometabolic diseases, suggesting BMI modifies these genetic effects.

This paper uses Mendelian randomization and colocalization to identify causal relationships between plasma proteins and disease phenotypes, finding 111 putatively causal effects.

This study uses Mendelian randomization to assess if antihypertensive drugs reduce Alzheimer’s disease risk by lowering systolic blood pressure, finding limited evidence of an effect.