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Mol Neurobiol. 2018 Mar;55(3):1847-1860. doi: 10.1007/s12035-017-0451-4. Epub 2017 Feb 22.

Involvement of Cellular Prion Protein in α-Synuclein Transport in Neurons.

Urrea L1,2,3,4, Segura-Feliu M1,2,3,4, Masuda-Suzukake M5, Hervera A1,2,3,4, Pedraz L6, García Aznar JM7, Vila M8,9, Samitier J10,11,12, Torrents E6, Ferrer I4,13,14,15, Gavín R1,2,3,4, Hagesawa M5, Del Río JA16,17,18,19.

Author information

1
Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Baldiri Reixac 15-21, E-08028, Barcelona, Spain.
2
Department of Cell Biology, Physiology and Immunology, Universitat de Barcelona, Barcelona, Spain.
3
Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Barcelona, Spain.
4
Institute of Neuroscience, University of Barcelona, Barcelona, Spain.
5
Department of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, 156-8506, Japan.
6
Bacterial infections: antimicrobial therapies. Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Barcelona, Spain.
7
Multiscale in Mechanical and Biological Engineering (M2BE), Aragon Institute of Engineering Research, Department of Mechanical Engineering, University of Zaragoza, Zaragoza, Spain.
8
Neurodegenerative Diseases Research Group, Vall d'Hebron Research Institute-Center for Networked Biomedical Research on Neurodegenerative Diseases, Autonomous University of Barcelona, Barcelona, Spain.
9
Catalan Institution for Research and Advanced Studies (ICREA), Barcelona, Spain.
10
Nanobioengineering Group, Institute for Bioengineering of Catalonia, (IBEC), Parc Científic de Barcelona, Barcelona, Spain.
11
Department of Electronics, University of Barcelona, Martí i Franquès 1, E-08028, Barcelona, Spain.
12
Centro de Investigación Biomédica en Red en Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029, Madrid, Spain.
13
Institut de Neuropatologia, IDIBELL-Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain.
14
Departamento de Patologia y Terapeutica Experimental, Facultad de Medicina, Universidad de Barcelona, Barcelona, Spain.
15
Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
16
Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Baldiri Reixac 15-21, E-08028, Barcelona, Spain. jadelrio@ibecbarcelona.eu.
17
Department of Cell Biology, Physiology and Immunology, Universitat de Barcelona, Barcelona, Spain. jadelrio@ibecbarcelona.eu.
18
Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Barcelona, Spain. jadelrio@ibecbarcelona.eu.
19
Institute of Neuroscience, University of Barcelona, Barcelona, Spain. jadelrio@ibecbarcelona.eu.

Abstract

The cellular prion protein, encoded by the gene Prnp, has been reported to be a receptor of β-amyloid. Their interaction is mandatory for neurotoxic effects of β-amyloid oligomers. In this study, we aimed to explore whether the cellular prion protein participates in the spreading of α-synuclein. Results demonstrate that Prnp expression is not mandatory for α-synuclein spreading. However, although the pathological spreading of α-synuclein can take place in the absence of Prnp, α-synuclein expanded faster in PrPC-overexpressing mice. In addition, α-synuclein binds strongly on PrPC-expressing cells, suggesting a role in modulating the effect of α-synuclein fibrils.

KEYWORDS:

Amyloid spreading; Microfluidic devices; Prnp; Synuclein

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