Gregor Wenning and Nadia Stefanova
Multiple system atrophy (MSA) is a fatal orphan disease that shares numerous features with PD including Parkinsonism and α-syuclein (α-syn) associated neurodegeneration. This group successfully established numerous rodent MSA models for pathogenic target identification and preclinical drug screening. Here we will characterize non-motor read-outs in transgenic (tg) MSA mice and also address the role of L-ype Ca2+ channels and epigenetic signalling changes in MSA-associated neurodegeneration.