Ellen J. Hess

The paper uses MoSeq to analyze behavioral changes in dystonia mouse models after trihexyphenidyl treatment, finding genotype and sex-specific shifts in behavioral structure.

The paper identifies cell-type-specific molecular changes in dystonia by analyzing translatomes of dSPNs and iSPNs in DRD mice, revealing glutamatergic signaling disruptions and identifying LRRK2 inhibition as a therapeutic target.

This study examines sensory deficits in a 6-OHDA-induced Parkinson's disease mouse model, revealing varied tactile sensation impairments alongside motor and dopaminergic changes.

This study shows that the Tor1a(ΔE) mutation in dopamine neurons reduces dopamine release, while having no effect in cholinergic neurons, indicating a cell-intrinsic role in dystonia.

The paper identifies differentially expressed proteins in a mouse model of DOPA-responsive dystonia, revealing shared mechanisms with human dystonic disorders.