Yiting Yuan

This study shows that juvenile AAV-mediated MEF2C gene replacement can improve specific phenotypes in Mef2c-haploinsufficient mice.

This study shows that AAV-mediated TBR1 replacement in Tbr1-haploinsufficient mice improves some behavioral and electrophysiological outcomes but not all abnormalities.

This study identifies an ASXL3-thyroid hormone axis in parvalbumin interneurons that regulates autism-like behaviors and shows that early TH supplementation can reverse these effects in mice.

This paper develops ProAPOBECs, engineered cytidine deaminases fused with PUF proteins, for effective RNA base editing in the brain, correcting mutations and reducing autistic-like behaviors in mice.

This study shows that AAV-mediated CSNK2B gene replacement in Csnk2b haploinsufficient mice rescues ASD-like phenotypes and restores EEG biomarkers, supporting its use as a translational readout for gene therapy.

This study shows that Srcap haploinsufficiency in mice causes autistic-like behaviors by reducing Satb2 expression, which can be reversed with Satb2 gene therapy.

This paper demonstrates whole-brain in vivo base editing in mice to reverse autistic-like behaviors by correcting a mutation in the MEF2C gene.

This study identifies a SENP1 mutation in mice that causes core autistic-like symptoms by disrupting the SENP1-FMRP axis in the retrosplenial agranular cortex.