RESEARCH ARTICLE Active immunization again n

Full list of author information is available at the end of the articleBackground Multiple system atrophy (MSA) is a progressive, neurode-generative disease characterized by parkinsonism resistant to dopamine therapy, ataxia, autonomic dysfunction, and pathological accumulation of α-synuclein (α-syn) [1-4]. MSA differs from other synucleinopathies in that α-syn ac-cumulates not only within neurons and astrocytes, but also within oligodendrocytes in the form of glial cytoplasmic inclusions [5]. This intracellular accumulation of toxic α-syn species leads to degeneration of oligodendroglial cells, loss of trophic support to neurons and subsequent neurodegeneration. In recent years increasing evidence supports the notion that α-syn is primarily generated by neurons, where it ag-gregates and gets released to the extracellular environ-ment [6,7]. Extracellular aggregated α-syn would then propagate to other neurons and glial cells in a prion-like fashion [8,9]. However, a recent report of MSA oligoden-drocytes also expressing α-syn mRNA [10] suggests that the origin of oligodendroglial α-syn might be both of en-dogenous nature and the result of propagation from neu