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Aggregation of the neuronal protein α-synuclein into insoluble filamentous inclusions may be a determining factor in the development of Parkinson disease (PD). Converging evidence has demonstrated that α-synuclein inclusions have prion-like properties, including cell-to-cell transmission and the ability to induce native α-synuclein to misfold, thus setting the stage for domino-like spreading of cellular pathology.1
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