Kayla G. Townsley

The paper evaluates estradiol's effects on ASD/NDD genes using human neurons and zebrafish, finding both convergent transcriptomic effects and gene-specific cellular and behavioral rescue.

The paper investigates how maternal and fetal immune activation interacts with genetic risk profiles to influence neuronal regulatory activity and psychiatric traits.

The paper develops a scalable framework to generate harmonized mtDNA datasets from existing sequencing data across biobanks, enabling population-scale mitochondrial genomics without new sequencing.

The paper maps R-loop landscapes in the developing human brain and shows their role in neural differentiation and gene expression programs.

The paper identifies BMI-dynamic gene expression loci in the brain and gut, showing how BMI interacts with genetic variants to influence gene expression and disease-related pathways.

This study identifies convergent biological pathways in mature neurons affected by neurodevelopmental disorder risk genes and shows drug candidates can ameliorate behavioral phenotypes.

The paper identifies stress-interactive eQTLs that dysregulate gene expression in the brain under stress, uncovering novel genes linked to brain disorder risk in traumatic stress contexts.

This study investigates the 3D genome organization in human brain development, finding differences in compartment and loop domain formation between neurons and glia.

The paper shows that non-additive effects of schizophrenia risk genes are due to convergent downstream transcriptomic effects and sub-additive changes, suggesting functional redundancy as a mechanism for non-additivity.

This study maps chromatin accessibility in Alzheimer's disease using ATAC-seq, identifying regulatory changes and 3D genomic alterations linked to disease.

The paper identifies population-level variation in enhancer expression in the human brain and links enhancer eQTL to schizophrenia heritability.

This study shows that schizophrenia risk genes have convergent and non-additive transcriptomic effects when perturbed together in human neurons, suggesting functional redundancy and complex interactions.

This study develops a method to efficiently generate dopaminergic neurons from hiPSCs and shows they model psychiatric disease risk genes.