Nadia Stefanova and Gregor K. Wenning
Multiple system atrophy (MSA) is a distinctive neurodegenerative disorder characterized by oligodendroglial cytoplasmic inclusions of fibrillar α-synuclein (α-syn) and associated with progressive multisystem neurodegeneration. Our group will provide detailed characterization of the functional phenotype of a transgenic mouse model with targeted overexpression of α-syn in oligodendrocytes as an important readout for preclinical drug screening for MSA. To identify underlying pathogenic mechanisms and candidate targets for future therapies we will focus on the putative bilateral interactions between epigenetic factors, and α-syn aggregation and propagation in MSA models. The outcomes are likely to critically enhance our insights into the pathogenesis and progression of MSA. The results will have immediate relevance for interventional target discovery which in turn will promote future clinical trial activities in MSA patients.