ChangHui Pak

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

This paper introduces a device to generate morphogen gradients for creating patterned brain organoids, revealing distinct cell types and long-term stability.

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 NRXN1 deletions affect brain development differently in specific cell types and genetic backgrounds, leading to synaptic dysfunction in organoids.

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 validates that heterozygous NRXN1 deletions impair neurotransmitter release in human neurons across multiple labs, suggesting a human-specific synaptic dysfunction relevant for schizophrenia drug discovery.