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. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: Mov Disord. 2017 Sep;32(9):1264–1310. doi: 10.1002/mds.27115

FIG. 8.

FIG. 8

(A) Schematic illustration of the similarity between the PrP and alpha-synuclein proteins in terms of their potential to misfold to form betarich sheets, and polymerize to form oligomers/rod, and amyloid plaques/Lewy Bodies (adapted from ref. 1). (B) Comparison of Lewy pathology in grafted embryonic dopamine neurons (graft) and in the host substantia nigra (host). Note the similarity in staining for alpha-synuclein, ubiquin, and thioflavin-S (indicative of beta sheet formation). These observations raise the possibility that misfolded alpha-synuclein has spread from affected neurons in the PD brain to unaffected implanted dopamine neurons in a prion-like manner (adapted from ref. 266).