It’s been nearly a decade since 
groups in the United States1 and Sweden2 reported alpha synuclein pathology in transplanted cells grafted into the brains of people with Parkinson’s disease. The Lewy body-like inclusions were accompanied by other markers of neuronal dysfunction that apparently developed over 10+ years. The pathology is remarkable because the transplanted cells were young and genetically unrelated to the individuals with Parkinson’s disease, suggesting an ongoing degenerative process in the parkinsonian brain and the presence of a pathological microenvironment.3
The finding of Lewy-like inclusions in transplanted cells led to the hypothesis that Parkinson’s disease could be a type of prion disease, involving the cell to cell transfer of misfolded alpha synuclein.2 Similarities between prion diseases and Parkinson’s disease had been documented in the literature since the early 1990s, but no pathology was observed in the prion protein involved in Creutzfeldt-Jakob’s disease.4 The observation of similarities persisted, though, and led to the concept of permissive templating–a process thought to be common to Parkinson’s, Creutzfeldt-Jakob’s, Alzheimer’s, Huntington’s, and other diseases of protein aggregation.5
