Ala Somarowthu

This study creates a mouse model with the KCNC1-A421V variant to investigate its effects on neuronal excitability and epilepsy, finding impaired function in fast-spiking interneurons and network dysfunction.

This study creates a mouse model of PMM2-CDG by selectively removing PMM2 from neural precursor cells, revealing cerebellar hypoplasia and ataxia, and showing molecular disturbances in the cerebellum that mirror human disease.

This study shows that electroconvulsive therapy (ECT) induces a postictal wave of spreading depolarization in both mice and humans, suggesting a new mechanism for its therapeutic effects.

This paper identifies and characterizes the SCN1A p.R1636Q gain-of-function variant, showing it causes early-onset epileptic encephalopathy with distinct clinical and electrophysiological features.

This study shows that impaired spike generation and synaptic transmission in parvalbumin interneurons contribute to Dravet syndrome severity and chronic pathology in an experimental model.

This study identifies circuit dysfunction in the hippocampus of a Dravet syndrome mouse model and shows that restoring parvalbumin interneuron function can rescue circuit impairments.