AUTHOR=Recasens Ariadna , Dehay Benjamin TITLE=Alpha-synuclein spreading in Parkinson’s disease JOURNAL=Frontiers in Neuroanatomy VOLUME=8 YEAR=2014 URL=https://www.frontiersin.org/journals/neuroanatomy/articles/10.3389/fnana.2014.00159 DOI=10.3389/fnana.2014.00159 ISSN=1662-5129 ABSTRACT=
Formation and accumulation of misfolded protein aggregates are a central hallmark of several neurodegenerative diseases. In Parkinson’s disease (PD), the aggregation-prone protein alpha-synuclein (α-syn) is the culprit. In the past few years, another piece of the puzzle has been added with data suggesting that α-syn may self-propagate, thereby contributing to the progression and extension of PD. Of particular importance, it was the seminal observation of Lewy bodies (LB), a histopathological signature of PD, in grafted fetal dopaminergic neurons in the striatum of PD patients. Consequently, these findings were a conceptual breakthrough, generating the “host to graft transmission” hypothesis, also called the “prion-like hypothesis.” Several