Alpha-synuclein propagation: New insights from animal models.

Benjamin Dehay, Miquel Vila, Erwan Bezard, Patrik Brundin, Jeffrey H. Kordower
Mov Disord.. 2015-09-08; 31(2): 161-168
DOI: 10.1002/mds.26370

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1. Mov Disord. 2016 Feb;31(2):161-8. doi: 10.1002/mds.26370. Epub 2015 Sep 8.

Alpha-synuclein propagation: New insights from animal models.

Dehay B(1)(2), Vila M(3)(4)(5), Bezard E(1)(2), Brundin P(6), Kordower JH(7).

Author information:
(1)Université de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293,
Bordeaux, France.
(2)CNRS, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux, France.
(3)Neurodegenerative Diseases Research Group, Vall d’Hebron Research Institute,
Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas, Barcelona,
(4)Department of Biochemistry and Molecular Biology, Autonomous University of
Barcelona, Bellaterra, Barcelona, Spain.
(5)Catalan Institution for Research and Advanced Studies, Barcelona, Spain.
(6)Laboratory for Translational Parkinson’s Disease Research, Center for
Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, Michigan,
(7)Department of Neurological Sciences, The Graduate College, Rush University,
Chicago, Illinois, USA.

Aggregation of alpha-synuclein is implicated in several neurodegenerative
diseases collectively termed synucleinopathies. Emerging evidence strongly
implicates cell-to-cell transmission of misfolded alpha-synuclein as a common
pathogenetic mechanism in synucleinopathies. The impact of alpha-synuclein
pathology on neuronal dysfunction and behavioral impairments is being explored in
animal models. This review provides an update on how research in animal models
supports the concept that misfolded alpha-synuclein spreads from cell to cell and
describes how findings in animal models might relate to the disease process in
humans. Finally, we discuss the current underlying molecular and cellular
mechanisms and future therapeutic strategies targeting alpha-synuclein

© 2015 International Parkinson and Movement Disorder Society.

DOI: 10.1002/mds.26370
PMID: 26347034 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus