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]