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Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 473706, 20 pages
Review Article

Evidence for Prion-Like Mechanisms in Several Neurodegenerative Diseases: Potential Implications for Immunotherapy

1Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Canada S7N 5E3
2Department of Biochemistry, University of Saskatchewan, Saskatoon, Canada S7N 5E5
3School of Public Health, University of Saskatchewan, Saskatoon, Canada S7N 5E5

Received 28 March 2013; Revised 11 June 2013; Accepted 2 July 2013

Academic Editor: Thierry Vincent

Copyright © 2013 Kristen Marciniuk et al. 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.


Transmissible spongiform encephalopathies (TSEs) are fatal, untreatable neurodegenerative diseases. While the impact of TSEs on human health is relatively minor, these diseases are having a major influence on how we view, and potentially treat, other more common neurodegenerative disorders. Until recently, TSEs encapsulated a distinct category of neurodegenerative disorder, exclusive in their defining characteristic of infectivity. It now appears that similar mechanisms of self-propagation may underlie other proteinopathies such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis, and Huntington’s disease. This link is of scientific interest and potential therapeutic importance as this route of self-propagation offers conceptual support and guidance for vaccine development efforts. Specifically, the existence of a pathological, self-promoting isoform offers a rational vaccine target. Here, we review the evidence of prion-like mechanisms within a number of common neurodegenerative disorders and speculate on potential implications and opportunities for vaccine development.