Kiran Girdhar

The paper maps gene expression, chromatin accessibility, and DNA methylation in developing human brain cells to understand regulatory interactions and their role in disease.

The paper introduces a probabilistic whitening transformation for high-dimensional genetic data, showing it is faster and more accurate than existing methods for imputing z-statistics and identifying genetic regulatory signals.

This study performs a single-nucleus transcriptome-wide association study to identify gene-trait associations in brain disorders, revealing cell-type-specific genetic regulation and ancestry-specific patterns.

The paper constructs a single-nucleus atlas of genetic regulation in the human brain, identifying cell-type-specific regulatory effects and disease-associated genes.

The paper constructs a single-cell transcriptomic atlas of the human dorsolateral prefrontal cortex across neurodegenerative and neuropsychiatric diseases, revealing shared and distinct molecular mechanisms.

This study identifies differential chromatin architecture and risk variants in specific brain cell types associated with major depressive disorder.

This study profiles small RNAs in schizophrenia and bipolar disorder, finding altered sncRNA abundance and links to accelerated aging and key biological processes.

This study creates a single-nucleus transcriptomic atlas of the human DLPFC across the lifespan, revealing three transcriptomic phases and ten age-related trajectories linked to neurodevelopmental and neurodegenerative disease risk.

The paper analyzes longitudinal blood transcriptomics in cocaine use disorder to identify gene co-expression networks and transcript associations linked to abstinence and relapse behaviors.

The paper identifies 46,802 enhancers and 164 psychiatric disorder variants with regulatory effects in the developing cortex and organoids using massively parallel reporter assays and deep learning.

The paper generates a molecular neuroanatomical map of the human prefrontal cortex using spatial transcriptomics and single nucleus RNA-sequencing, revealing novel spatial domains and cell-cell interactions linked to psychiatric disorders.

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

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.

The paper identifies regulatory mechanisms for 21 Alzheimer's disease risk loci in human microglia using transcriptome and chromatin accessibility profiling.

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.

The paper identifies acetylated chromatin domains associated with dysfunction in schizophrenia and bipolar disorder by analyzing histone modifications in prefrontal cortex samples.

This paper performs a large-scale eQTL meta-analysis across cerebral cortical and cerebellar brain regions, identifying distinct eQTL patterns and demonstrating improved power over existing studies.

The paper functionally annotates rare structural variants in the human brain by integrating SV calling with RNA-seq data to assess their regulatory effects and prioritize pathogenic deletions.

The paper identifies SNRNP35 as a trauma type-specific PTSD gene through analysis of genetically regulated gene expression in PTSD cases and controls.

The paper uses transcriptomic imputation to identify schizophrenia risk genes across multiple brain regions, finding 71 associated genes and 36 enriched pathways.

The paper integrates GWAS and conditional eQTL data to identify schizophrenia risk loci with co-localization, finding 40 loci and six with conditional eQTL co-localization.