Morgan J. Robinson

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

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 uses high-speed AFM to examine how amyloid-β and cholesterol affect the dynamic stability of lipid domains in model membranes.

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.

The paper develops an all-RNA prime editing system achieving over 95% editing efficiency in human iPSCs with minimal off-target effects.

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.