Andrew D. Nelson

This study shows that CRISPR activation can rescue electrophysiological deficits in SCN2A haploinsufficiency by increasing the expression of the remaining functional allele in mice and human neurons.

The paper identifies impaired cerebellar plasticity as a mechanism underlying hypersensitized sensory reflexes in SCN2A-associated ASD, showing that increasing Scn2a expression rescues VOR plasticity in mice.

This study shows that Ank2 and Scn2a work together in dendrites of neocortical neurons, linking their dysfunction to autism spectrum disorder.

This paper investigates the effects of the SCN2A p.K1422E variant in mice, showing mixed functional and behavioral impacts on neurons and neurodevelopmental phenotypes.

This study shows that ankyrin-G regulates forebrain connectivity and network synchronization through its interaction with GABARAP, and identifies a variant linked to bipolar disorder.