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Neurology Research International
Volume 2015 (2015), Article ID 345285, 8 pages
Review Article

Is Parkinson’s Disease Truly a Prion-Like Disorder? An Appraisal of Current Evidence

1Hertford College, University of Oxford, Catte Street, Oxford OX1 3BW, UK
2Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK

Received 26 August 2014; Accepted 16 December 2014

Academic Editor: Changiz Geula

Copyright © 2015 Aneesha Chauhan and Alexander F. Jeans. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Parkinson’s disease (PD) is the world’s second most common neurodegenerative disease and most common movement disorder. Characterised by a loss of dopaminergic neurons and the development of intraneuronal inclusions known as Lewy bodies, it has classically been thought of as a cell-autonomous disease. However, in 2008, two groups reported the startling observation of Lewy bodies within embryonic neuronal grafts transplanted into PD patients little more than a decade previously, suggesting that PD pathology can be propagated to neighbouring cells and calling basic assumptions of our understanding of the disease into question. Subsequent research has largely served to confirm this interpretation, pointing towards a prion-like intercellular transfer of misfolded α-synuclein, the main component of Lewy bodies, as central to PD. This shift in thinking offers a revolutionary approach to PD treatment, potentially enabling a transition from purely symptomatic therapy to direct targeting of the pathology that drives disease progression. In this short review, we appraise current experimental support for PD as a prion-like disease, whilst highlighting areas of controversy or inconsistency which must be resolved. We also offer a brief discussion of the therapeutic implications of these discoveries.