Genetic mutation in SCN2A has been found to be a leading cause of monogenic autism and epilepsy. SCN2A encodes the voltage-gated sodium channel Nav1.2, a key mediator
of neuronal action potential firing in the brain. In this lecture, Dr. Yang will discuss how SCN2A deficiency and genetic mutation affect neuronal and circuit functions as well as animal behaviors in disease models. Dr. Yang will also discuss the development of potential genetic medicine, including gene augmentation therapy and advanced CRISPR Prime Editing for disease interventions of SCN2A-related brain disorders.
