Elliot M. Tucker–Drob

The paper examines how polygenic indices for educational attainment change across birth cohorts and regions in Germany, finding stronger associations in recent cohorts and the East but weaker effects for women.

The paper shows that general cognitive function is supported by a widespread white matter network across multiple brain regions and connectivity measures.

The paper introduces an ultra-fast analytic solution for multivariate GWAS in Genomic SEM, reducing computation time by over 800 times and enabling efficient analysis on standard hardware.

This study identifies 1,294 genomic regions and 961 effector genes associated with externalizing disorders, revealing neural mechanisms and polygenic predictors of variance in these conditions.

The paper introduces an effect size index and automated functions to assess specific genetic associations between external traits and common factors, applied to cognitive ability and Alzheimer's disease indicators.

This paper introduces new graph measures for brain structural connectomes, showing they better predict general cognitive function than existing measures.

This paper evaluates methods to estimate lifetime brain atrophy from a single MRI scan and identifies genetic correlates, finding that the residual method best captures brain shrinkage and has strong heritability.

The paper updates a polygenic index repository with more phenotypes, datasets, and improved causal inference methods, enhancing predictive performance and interpretability.

This study evaluates transdiagnostic polygenic risk scores for psychiatric disorders using the All of Us Research Program data, finding that a common psychiatric genetic factor PRS better predicts comorbidity burden than single-disorder scores.

The paper compares the multivariate genetic architecture of eight psychiatric disorders between males and females using Genomic Structural Invariance, finding similarities and sex-specific differences in genetic factor loadings.

The paper introduces GTACCC to assess genetic continuity and differentiation of negative emotionality and MDD across severity, finding increasing genetic sharing with severity.

The paper identifies five genomic factors explaining most genetic variance across 14 psychiatric disorders and finds shared and disorder-specific genetic signals with distinct biological functions.

Family-based GWAS meta-analysis of 34 phenotypes shows standard GWAS effects carry sizeable confounding uncorrelated with direct genetic effects, while assortative mating likely inflates SNP heritability and genetic correlations.

The paper finds stronger polygenic associations with educational attainment in East Germans after reunification compared to West Germans.

The paper identifies general and specific patterns of cortical gene expression related to cognitive functioning using principal component analysis and validates them across datasets.

The paper describes the Gene-SOEP dataset, a longitudinal genetic study of 2,598 individuals in Germany, providing polygenic indices for research on genetic-environment interactions.

This study examines the stability of DNA-methylation profiles of biological aging in children and adolescents over four years, finding moderate stability and less stability compared to adults.

The paper uses deep learning on DXA images to identify genetic variants affecting skeletal proportions and links these to evolutionary changes and disease risk.

This study identifies genetic subtypes of major depressive symptoms by analyzing data from clinical and community cohorts, finding distinct factors for appetite/weight symptoms and missing data patterns.

This study shows noncognitive skills become more predictive of academic achievement over time and their genetic contribution increases with age.

This study uses genomic PCA to identify shared genetic architecture between brain morphometry, ageing, and cognitive ability using UK Biobank data.

This study shows that epigenetic-BMI measured from children's saliva is a valid biomarker of BMI and reflects social inequalities in childhood and adolescence.

The paper shows that standard methods for liability-scale heritability estimation in GWAS meta-analysis can be downwardly biased and proposes a simple correction based on effective sample size summation.

The paper tests if socioeconomic gradients observed in blood DNA methylation measures can be reproduced using buccal-cell DNA, finding smaller effect sizes and lower cross-tissue correlations.

The paper examines DNA-methylation profiles in children and adolescents, finding associations between social inequality and epigenetic markers of inflammation, cognitive functioning, and biological aging.

This study performs a multivariate GWAS on psychiatric disorders and symptoms to identify two genetic liabilities distinguishing common mood disturbances from serious mental illnesses.

This study identifies four genetic factors underlying 11 psychiatric disorders and finds limited evidence for a single dimension of genetic risk across them.

This study identifies DNA methylation predictors of cognitive function using blood samples, showing they explain variance in cognitive ability and associate with biological markers.

The paper develops epigenetic scores (EpiScores) for plasma proteins to predict disease risk, finding 137 associations with incident morbidities independent of known factors.

The paper constructs polygenic indexes for 47 phenotypes across 11 datasets and provides a tool to correct errors-in-variables bias when using PGIs as proxies for the additive SNP factor.