Zhexing Wen

This paper develops a detergent-free method to produce Aβ42 oligomers compatible with solid-state NMR and shows they induce stronger microglial inflammation than monomers.

This study identifies dysregulated synaptic microRNAs in 22q11DS neurons that drive aberrant glutamatergic transmission and synaptic plasticity, linking genetic deletion to psychosis risk.

The paper investigates how neurodevelopmental disorder-associated variants affect mitochondrial proteins and finds convergent effects on mitochondrial translation in two high-risk CNVs.

The paper presents a cell type-resolved proteomic atlas of Alzheimer's disease mouse models, identifying thousands of cell-specific protein changes and highlighting astrocyte-microglia signaling.

scCotag improves single-cell multi-omics integration by using co-optimal transport and regularized barycentric mapping, outperforming existing methods in alignment and embedding accuracy.

This study uses longitudinal multi-omics analysis of cortical organoids to show that TSC2 pathogenic variants disrupt neurodevelopmental trajectories, leading to synaptic and mitochondrial dysfunction.

This study investigates GABAergic neuron dysfunction in psychiatric disorder models, finding mutation-dependent synaptic deficits and shared gene expression changes in DISC1 mutant neurons.

This paper develops a mesofluidic bioreactor platform with high-content imaging for non-invasive quality control of brain organoids, improving their development and reducing cell death.

Deep5hmC predicts genome-wide 5hmC modification using a multimodal deep learning model, outperforming unimodal models and existing methods in both qualitative and quantitative predictions.

This study shows that FMRP phosphorylation regulates neuronal translation via YTHDF1, revealing a mechanism for FXS pathology and suggesting YTHDF1 as a therapeutic target.

This study uses cross-species scRNA-seq to show that the 3q29 deletion causes mitochondrial dysfunction in both human cortical organoids and mouse models, suggesting a conserved metabolic disruption in schizophrenia.

The paper identifies five core protein kinases in neurons and astrocytes from familial AD patient iPSCs and examines their enriched pathways using a combination of experimental and in-silico approaches.

The paper shows that mitochondrial proteostasis genes in a neurodevelopmental syndrome locus are essential for synapse function and behavior in Drosophila.

This study investigates the molecular effects of the 3q29 deletion on the human neural transcriptome, identifying convergent and distributed impacts across gene clusters and pathways related to psychiatric disorders.

This study evaluates 32 individuals with 3q29 deletion syndrome to identify common medical and neurodevelopmental features and provides clinical care recommendations.

The paper develops an improved Hi-C protocol and bias-correction pipeline to map chromatin loops in human neurogenesis and brain tissues, showing their role in neural differentiation and GWAS gene identification.

The paper identifies PPAR agonists as potential treatments for schizophrenia by analyzing bioenergetic changes in the DLPFC using bioinformatics and experimental validation.

The paper identifies a mitochondrial transporter interactome disruption in 22q11.2 syndrome, linking it to synapse function and behavior.

This study identifies virus- and strain-specific molecular signatures of ZIKV infection in human cortical neural progenitors, showing distinct impacts on DNA replication and apoptosis.