Zhiping P. Pang

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

The paper develops and validates polygenic scores for substance use disorders across multiple ancestries, finding clinically relevant performance in European and Latinx populations but not in African populations.

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

This study analyzes 173 multiplex Portuguese families to identify rare genetic variants associated with schizophrenia, mood disorders, and autism, finding a CHD2 mutation linked to diverse mental illness phenotypes.

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 identifies AKAP11 as a critical autophagy receptor linking PKA kinase network regulation to synaptic transmission, with loss-of-function impacting pathways associated with bipolar disorder and schizophrenia.

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 synaptic effects of NRXN1 deletions in ASD and SCZ iPSC models, finding distinct synaptic and network impairments in ASD.

The paper quantifies viscoelastic properties of synapsin condensates in live cells and identifies α-synuclein's role in regulating their material state.

This paper develops a high-throughput method to measure neuronal activity in human iPSC-derived glutamatergic neurons using Mg2+-free ACSF and confirms donor-specific firing patterns.

This study develops a method to generate diverse GABAergic neurons from PSCs using TFs and signaling inhibition, showing distinct subtype compositions and disease relevance.

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

This study shows that loss of MARK2 in vivo causes dendritic spine changes, reduced excitatory transmission, and behavioral impairments, including seizures and cognitive deficits.

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 uses multiomic profiling of the caudate nucleus to identify gene expression and chromatin changes in AUD, linking them to risk genes through QTL analysis.

This study shows that loss of Par3 increases long, thin dendritic spines and enhances hippocampal-dependent learning and memory in vivo.

This study identifies dLSGLP-1R neurons and their GABAergic projections to the LHA as regulators of feeding behavior in mice, showing that inhibition of these pathways increases food intake.

The paper investigates how upregulated GIRK2 affects ethanol-induced changes in human neurons, showing it counteracts excitability and respiration changes.

This study shows that a specific AAV-Cre preparation causes toxicity in the PVN, leading to metabolic and behavioral changes, independent of genetic background.

This study shows HIV-1 infects human iPSC-derived microglia, causing sustained type I interferon signaling and disease risk gene expression in a neural model.

The paper investigates the impact of the NLGN3 R451C mutation on human neurons, finding it reduces protein levels but enhances excitatory synapses, potentially contributing to ASD pathogenesis.

This study shows that KCNJ6 noncoding variants increase excitability in human glutamatergic neurons, an effect reversed by ethanol exposure.

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.

This study shows that CASK loss disrupts synaptic transmission and network synchronicity in mature human cortical neurons but not synapse formation or neurite complexity.

This study identifies MCH's role in enhancing synaptic transmission in the hippocamposeptal circuit to improve spatial memory through modulation of excitatory and inhibitory mechanisms.

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