Aggregation of alpha synuclein (αsyn) and related toxicities play a central role in the development of Parkinson’s disease, dementia with Lewy bodies, multiple system atrophy and several neurodegenerative disorders, collectively referred as synucleinopathies. Recently, oligomeric and pre-fibrillar forms of αsyn have been identified as the toxic species in Parkinson’s disease. Until recently, αsyn was thought to exert its toxic effects intracellularly. However, new data support an alternative possibility: that some forms of αsyn are secreted from, and taken up by neurons, and that this extracellular αsyn may be a toxic species. Our goal is to understand the underlying mechanisms of secretion, uptake of αsyn oligomers into neighboring neurons and propagation of αsyn pathology. Our special interest is not only the exosomal secretion of αsyn oligomers but also additional key proteins in neurodegenerative disorders like Aß, Tau und SOD1. Using a wealth of biochemical, cell biological and molecular approaches, as well as analysis of patient samples and establishing new animal models we hope to understand underlying disease mechanisms and to identify not only new biomarkers but also additional and new factors contributing to neurodegeneration.