Gene-environment interaction elicits dystonia-like features and impaired translational regulation in a DYT-TOR1A mouse model (RNA-Seq)
To elicit a dystonia-like phenotype in a genetically predisposed DYT-TOR1A mouse model (DYT1KI) by performing a right sciatic nerve crush injury. To identify novel pathophysiological pathways and possible biomarker, we performed a multi-omic analysis of three dystonia-relevant brain regions Overall design: Comparative gene expression profiling analysis of RNA-seq data for the cortex, striatum and cerebellum of naive and nerve-injured wildtype and DYT1KI mice