What’s to like about the prion-like hypothesis for the spreading of aggregated α-synuclein in Parkinson disease? |
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Authors: | Christopher JR Dunning Sonia George Patrik Brundin |
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Institution: | 1Neuronal Survival Unit; Wallenberg Neuroscience Center; Lund University; Lund, Sweden;2Van Andel Research Institute; Center for Neurodegenerative Science; Grand Rapids, MI USA |
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Abstract: | α-Synuclein is a key protein in Parkinson disease. Not only is it the major protein component of Lewy bodies, but it is implicated in several cellular processes that are disrupted in Parkinson disease. Misfolded α-synuclein has also been shown to spread from cell-to-cell and, in a prion-like fashion, trigger aggregation of α-synuclein in the recipient cell. In this mini-review we explore the evidence that misfolded α-synuclein underlies the spread of pathology in Parkinson disease and discuss why it should be considered a prion-like protein. |
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Keywords: | Parkinson disease alpha-synuclein cell-to-cell transfer prion-like protein misfolding |
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