Jubao Duan

PULSE, a foundation model trained on neural recordings, reveals how disease variants affect network development and how circuits encode information in brain organoids.

This study examines how different SETD1A mutations and genetic backgrounds affect human hippocampal neurons derived from hiPSCs, revealing divergent molecular and cellular phenotypes and contrasting mutation impacts.

This study identifies AUD-associated and ethanol-responsive proteins in human cortical organoids and finds candidate biomarkers linked to AUD and ethanol exposure.

The paper identifies context-specific genetic effects in neuronal activation using single-cell multiomics, revealing NPD risk variants and genes active during stimulation.

The paper investigates XCI erosion in CRISPR-edited female iPSCs and their derived neurons, showing variable erosion in iPSCs and preserved XIST effects on gene expression in neurons.

This study shows ethanol exposure in a human iPSC-derived triculture model increases TREM2 expression and soluble TREM2 through alternative splicing, suggesting a link to neuroimmune dysregulation in alcohol use disorders.

This study compares the effects of intermittent hypoxia and hypoxia-ischemia models on myelination in neonatal mice using spatial transcriptomics, finding region-specific differences in oligodendrocyte populations and inflammatory responses.

The paper investigates DNA breathing's role in TF-DNA interactions using in vitro and in vivo data, finding correlations between breathing features near motifs and binding affinity across multiple TFs.

This study examines how polygenic risk scores for Alcohol Use Disorder affect microglial responses to ethanol exposure in human iPSC-derived microglia.

This study investigates how rare mutations in the SETD1A gene affect human neurons, showing they disrupt synaptic function and may contribute to schizophrenia pathophysiology.

The paper develops a pipeline for efficient loss-of-function mutagenesis in NPD genes using base editing in hiPSCs, achieving high reproducibility and confirming neural phenotypes.

The paper identifies an AD protective allele of CLU that enhances neuronal excitability via lipid-droplet-mediated neuron-glia communication.

The paper identifies genetically distinct patient subgroups across diseases by analyzing polygenic risk and pathway convergence.

The paper uses brain cell-type-specific protein interactomes to interpret genetic data in schizophrenia and identifies enriched networks and genes associated with the disease.

The paper identifies OTUD7A loss-of-function mutations in schizophrenia-associated 15q13.3 deletions and shows they impair synapse development and function in human neurons.

A genome-wide association study of 69,369 schizophrenia cases and 236,642 controls identifies 270 risk loci, prioritizes 130 genes, and links common and rare risk variants to neuronal synaptic biology.

This study identifies sex-dependent genetic risk loci shared and specific to mood and psychotic disorders using genome-wide interaction analysis.

The paper identifies multiple genes in cis regulated by a chromatin accessibility variant that contribute to synaptic dysfunction in human neurons associated with schizophrenia.

The paper compares ten polygenic score methods for psychiatric disorders across multiple cohorts, finding that some methods significantly improve prediction statistics over the baseline PC+T method.

CellR imputes cell type-specific expression profiles and cellular compositions from bulk RNA-Seq data in brain disorders, showing improved accuracy and stability compared to existing methods.

The paper introduces MetaChrom, a deep transfer learning framework for predicting epigenomic functions of genetic variants in neurodevelopment, showing improved accuracy over existing methods.

The paper introduces a method to integrate multi-omics data for predicting schizophrenia risk genes by modeling proteogenomic signal diffusion across cell types and tissues.

The paper presents twelve hiPSC lines with extreme polygenic risk scores for schizophrenia, available for CRISPR-based functional studies.

The paper identifies allele-specific open chromatin (ASoC) variants in human iPSC-derived neurons and shows their strong enrichment in brain disorder risk variants.

The paper introduces CCmed methods to detect robust trans-eQTLs and assess their effects on human traits by analyzing brain tissue data from GTEx and validating findings with schizophrenia GWAS data.

The paper deconvolves transcriptional networks in schizophrenia to identify TCF4 as a master regulator potentially dysregulated in the disease.

SummaryAUC approximates the AUC of polygenic risk scores using only summary statistics from validation datasets, enabling efficient evaluation of PRS models.

This study identifies PPP1R3F as a master regulator in ASDs using network deconvolution and RNA-Seq data from cerebellum samples.

The paper finds a genetic association between schizophrenia risk and age at first birth in women, with different genetic correlations in younger and older age groups.