Shani Stern

Zuckerman Faculty Scholar Shani Stern published a study, Shank3 mutation impairs glutamate signaling and myelination in ASD mouse model and human iPSC-derived OPCs, in Science Advances. The study advances the understanding of biological mechanisms behind genetic autism, and found that SHANK3 protein mutations disrupt brain development, which may contribute to autism. Stern conducted the study in collaboration with researchers from Tel Aviv University.

Abstract:
Autism spectrum disorder (ASD) is characterized by social and neurocognitive impairments, with mutations of the SHANK3 gene being prominent in patients with monogenic ASD. Using the InsG3680 mouse model with a Shank3 mutation seen in humans, we revealed an unknown role for Shank3 in postsynaptic oligodendrocyte (OL) features, similar to its role in neurons. Our study provides insight into Shank3’s role in OLs and reveals a mechanism of the crucial connection of myelination to ASD pathology.