Brody A. Deming

This study shows that Scn2a-deficient mice have altered serotonergic function and different behavioral responses to psilocybin compared to wild-type mice.

This study shows that inducing Kv1.1 expression in Scn2a-deficient mice reduces neuronal hyperexcitability and improves sociability without affecting wild-type mice.

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 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 shows that restoring NaV1.2 expression in adulthood rescues social deficits and improves neuronal signal-to-noise ratio in Scn2a-deficient mice.

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.