Matthew C. Weston

This study shows PTEN regulates neuronal growth and excitability through distinct mTORC1 and mTORC2 pathways, with implications for ASD and epilepsy.

This study shows that both mTORC1 and mTORC2 hyperactivity contribute to epilepsy caused by somatic PTEN loss, and that inhibiting both complexes can normalize brain activity.

This study examines how a KCNT1 gain-of-function variant affects SST and PV GABAergic neurons, revealing differential functional outcomes and potential pathogenic mechanisms in DEEs.

This study identifies that excess interictal activity marks seizure-prone cortical areas in a genetic epilepsy model, with altered activity intensity predicting seizure burden.

The paper investigates how a gain-of-function K+ channel variant causes seizures by reducing inhibitory neuron excitability and increasing network hyperconnectivity.

This study investigates the distinct roles of mTORC1 and mTORC2 in glutamatergic synaptic transmission by genetically inactivating each complex in mouse neurons, revealing their specific effects on presynaptic and postsynaptic functions.