Review Article
Evidence for Prion-Like Mechanisms in Several Neurodegenerative Diseases: Potential Implications for Immunotherapy
Table 1
Evidence for prion-like mechanisms in common neurodegenerative disorders.
| Disease | Misfolded protein | Aggregate cellular location | Self-propagation | Cell-cell spread | Tissue migration | Transmission | Resistance to degradation |
| TSEs | Prion | Intracellular [33] Extracellular [34] | Yes | Yes | Yes | Yes | Yes | Alzheimer’s | Amyloid beta | Intracellular [35] Extracellular [36] | Yes [37] | Yes [38] | Yes [39–41] | Yes [39, 42, 43] | Yes [44, 45] | Alzheimer’s | Tau | Intracellular [46] Extracellular [47, 48] | Yes [49] | Yes [50–52], | Yes [53, 54] | Yes [43, 55] | Yes [56, 57] | Parkinson’s | α-Synuclein | Intracellular [58] Extracellular [59, 60] | Yes [59] | Yes [59, 61–65] | Yes [62, 66] | Possibly [66] | Yes [67, 68] | ALS | SOD1 | Intracellular [69] Extracellular [70] | Yes [71, 72] | Yes [73] | Possibly [74] | No | No ↑ degradation [75, 76] | ALS | TDP-43 | Intracellular [77] | Yes [78] | No | No | No | No | Huntington’s | Huntingtin | Intracellular [79] | Yes [78, 80, 81] | Possibly [80] | Possibly [82] | No | Yes [83] |
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