Wei‐Dong Yao

This study introduces a behavioral paradigm to assess disinhibition in a mouse model of frontotemporal dementia, identifying specific neural circuits involved in self-control.

This study shows that IL-NAcSh neurons suppress cocaine-associated memories through reduced excitability after cocaine exposure, and restoring their activity can extinguish these memories.

This study shows that elevating neuronal CYLD causes FTD-like behavioral and physiological deficits in mice, with M719V mutation acting as a gain-of-function.

This study identifies USP48 as a nuclear deubiquitinase that regulates synapse remodeling by promoting spine pruning and reducing synaptic protein clustering.

This study shows CYLD promotes synapse pruning and weakening via Akt-mTOR-autophagy signaling, leading to behavioral and synaptic deficits in mice.