Chongli Yuan

This study shows that SCN2A deficiency in human brain assembloids disrupts cortico-striatal circuitry by impairing axonal projections and synaptic transmission, leading to hyperexcitability.

The paper develops a chemoselective bioconjugation method to detect and analyze NEylation, revealing it as a widespread PTM affecting protein function in cells.

This study uses snRNA-seq to analyze gene expression changes in Scn2a-deficient mice, identifying disrupted pathways in neuronal subtypes of the prefrontal cortex.

This study investigates the effects of the SCN2A-L1342P mutation in human cortical organoids, finding increased neuronal excitability, enhanced synaptic transmission, and transcriptomic changes related to synaptic and developmental pathways.

This study develops a human neuronal chimera model to study Alzheimer's tau pathology, showing human-specific vulnerability and recapitulating mature AD features in vivo.

This study constructs cell-type-specific gene regulatory networks in Alzheimer's disease using single-nucleus transcriptomics and genotype data, identifying both established and novel regulatory elements.

The paper predicts neuronal subtype-specific metabolic changes in neurodegenerative and neuropsychiatric diseases using a systems biology approach and integrates metabolic networks with single nucleus RNA sequencing data.

This study uses brain organoids and assembloids with microglia to show region-specific microglial diversity and their response to SCN2A mutation-induced neuronal hyperactivity.

This paper shows that gene therapies can reduce absence seizures in DBA/2J mice with Scn2a deficiency by restoring NaV1.2 or introducing human KV1.1.

This study uses vascularized neuroimmune organoids to model sporadic Alzheimer's disease and test drug efficacy.

This study identifies Kir7.1's role in maintaining membrane potential and directional sensing during neutrophil chemotaxis, showing its necessity for polarized depolarization and chemotactic movement.

This study shows human iPSC-derived microglia detect and reduce hyperexcitability in neurons with the SCN2A-L1342P epilepsy mutation through morphological and calcium changes and reduced sodium channel current density.

The paper investigates how nucleosome positioning elements and pre-assembled chromatin states affect transgene expression and retention, finding that nucleosome positioning has a greater impact than hyperacetylated chromatin states.

This study shows that severe NaV1.2 deficiency increases neuronal excitability in adult mice, challenging the current understanding of its role in autism and epilepsy.

This study shows that low-dose lead exposure alters heterochromatin marks in SH-SY5Y cells, with some changes persisting through differentiation and affecting neuronal morphology.