Gene-environment interaction elicits dystonia-like features and impaired translational regulation in a DYT-TOR1A mouse model (miRNA-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 miRNA expression profiling analysis of miRNA-seq data for the cortex, striatum and cerebllum of naive and nerve-injured wildtype and DYT1KI mice