Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an AAV-Based Rat Genetic Model of Parkinson’s Disease
Identifieur interne : 000233 ( Pmc/Checkpoint ); précédent : 000232; suivant : 000234Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an AAV-Based Rat Genetic Model of Parkinson’s Disease
Auteurs : Abid Oueslati [Suisse, Canada] ; Blaise Lovisa [Suisse] ; John Perrin [Suisse] ; Georges Wagnières [Suisse] ; Hubert Van Den Bergh [Suisse] ; Yanik Tardy [Suisse] ; Hilal A. Lashuel [Suisse, Qatar]Source :
- PLoS ONE [ 1932-6203 ] ; 2015.
Abstract
Converging lines of evidence indicate that near-infrared light treatment, also known as photobiomodulation (PBM), may exert beneficial effects and protect against cellular toxicity and degeneration in several animal models of human pathologies, including neurodegenerative disorders. In the present study, we report that chronic PMB treatment mitigates dopaminergic loss induced by unilateral overexpression of human α-synuclein (α-syn) in the substantia nigra of an AAV-based rat genetic model of Parkinson’s disease (PD). In this model, daily exposure of both sides of the rat’s head to 808-nm near-infrared light for 28 consecutive days alleviated α-syn-induced motor impairment, as assessed using the cylinder test. This treatment also significantly reduced dopaminergic neuronal loss in the injected substantia nigra and preserved dopaminergic fibers in the ipsilateral striatum. These beneficial effects were sustained for at least 6 weeks after discontinuing the treatment. Together, our data point to PBM as a possible therapeutic strategy for the treatment of PD and other related synucleinopathies.
Url:
DOI: 10.1371/journal.pone.0140880
PubMed: 26484876
PubMed Central: 4617694
Affiliations:
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AAV-Based Rat Genetic Model of Parkinson’s Disease</title><author><name sortKey="Oueslati, Abid" sort="Oueslati, Abid" uniqKey="Oueslati A" first="Abid" last="Oueslati">Abid Oueslati</name><affiliation wicri:level="3"><nlm:aff id="aff001"><addr-line>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland</addr-line></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne</wicri:regionArea><placeName><settlement type="city">Lausanne</settlement><region nuts="3" type="region">Canton de Vaud</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>Centre de Recherche du Centre Hospitalier de Québec, Axe Neuroscience et Département de Médecine Moléculaire de l'Université Laval, 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Lashuel</name><affiliation wicri:level="3"><nlm:aff id="aff001"><addr-line>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland</addr-line></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne</wicri:regionArea><placeName><settlement type="city">Lausanne</settlement><region nuts="3" type="region">Canton de Vaud</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff005"><addr-line>Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. Box 5825, Doha, Qatar</addr-line></nlm:aff><country xml:lang="fr">Qatar</country><wicri:regionArea>Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. Box 5825, Doha</wicri:regionArea><wicri:noRegion>Doha</wicri:noRegion></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Converging lines of evidence indicate that near-infrared light treatment, also known as photobiomodulation (PBM), may exert beneficial effects and protect against cellular toxicity and degeneration in several animal models of human pathologies, including neurodegenerative disorders. In the present study, we report that chronic PMB treatment mitigates dopaminergic loss induced by unilateral overexpression of human α-synuclein (α-syn) in the substantia nigra of an AAV-based rat genetic model of Parkinson’s disease (PD). In this model, daily exposure of both sides of the rat’s head to 808-nm near-infrared light for 28 consecutive days alleviated α-syn-induced motor impairment, as assessed using the cylinder test. This treatment also significantly reduced dopaminergic neuronal loss in the injected substantia nigra and preserved dopaminergic fibers in the ipsilateral striatum. These beneficial effects were sustained for at least 6 weeks after discontinuing the treatment. Together, our data point to PBM as a possible therapeutic strategy for the treatment of PD and other related synucleinopathies.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Obeso, Ja" uniqKey="Obeso J">JA Obeso</name></author><author><name sortKey="Rodriguez Oroz, Mc" uniqKey="Rodriguez Oroz M">MC Rodriguez-Oroz</name></author><author><name sortKey="Goetz, Cg" uniqKey="Goetz C">CG Goetz</name></author><author><name sortKey="Marin, C" uniqKey="Marin C">C Marin</name></author><author><name sortKey="Kordower, Jh" uniqKey="Kordower J">JH Kordower</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dauer, W" uniqKey="Dauer W">W Dauer</name></author><author><name sortKey="Przedborski, S" uniqKey="Przedborski S">S Przedborski</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lashuel, Ha" uniqKey="Lashuel H">HA Lashuel</name></author><author><name sortKey="Overk, Cr" 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<front><journal-meta><journal-id journal-id-type="nlm-ta">PLoS One</journal-id><journal-id journal-id-type="iso-abbrev">PLoS ONE</journal-id><journal-id journal-id-type="publisher-id">plos</journal-id><journal-id journal-id-type="pmc">plosone</journal-id><journal-title-group><journal-title>PLoS ONE</journal-title></journal-title-group><issn pub-type="epub">1932-6203</issn><publisher><publisher-name>Public Library of Science</publisher-name><publisher-loc>San Francisco, CA USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26484876</article-id><article-id pub-id-type="pmc">4617694</article-id><article-id pub-id-type="doi">10.1371/journal.pone.0140880</article-id><article-id pub-id-type="publisher-id">PONE-D-15-29778</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an AAV-Based Rat Genetic Model of Parkinson’s Disease</article-title><alt-title alt-title-type="running-head">PBM Suppresses α-Synuclein Toxicity <italic>In Vivo</italic></alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Oueslati</surname><given-names>Abid</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref><xref ref-type="aff" rid="aff002"><sup>2</sup></xref><xref rid="cor001" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Lovisa</surname><given-names>Blaise</given-names></name><xref ref-type="aff" rid="aff003"><sup>3</sup></xref><xref ref-type="aff" rid="aff004"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Perrin</surname><given-names>John</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wagnières</surname><given-names>Georges</given-names></name><xref ref-type="aff" rid="aff003"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>van den Bergh</surname><given-names>Hubert</given-names></name><xref ref-type="aff" rid="aff003"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Tardy</surname><given-names>Yanik</given-names></name><xref ref-type="aff" rid="aff004"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lashuel</surname><given-names>Hilal A.</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref><xref ref-type="aff" rid="aff005"><sup>5</sup></xref><xref rid="cor001" ref-type="corresp">*</xref></contrib></contrib-group><aff id="aff001"><label>1</label><addr-line>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland</addr-line></aff><aff id="aff002"><label>2</label><addr-line>Centre de Recherche du Centre Hospitalier de Québec, Axe Neuroscience et Département de Médecine Moléculaire de l'Université Laval, Québec, G1V4G2, Canada</addr-line></aff><aff id="aff003"><label>3</label><addr-line>Institute of Chemical Sciences and Engineering, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland</addr-line></aff><aff id="aff004"><label>4</label><addr-line>Medos International Sàrl, a Johnson&Johnson company, Chemin Blanc 38, CH-2400, Le Locle, Switzerland</addr-line></aff><aff id="aff005"><label>5</label><addr-line>Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. Box 5825, Doha, Qatar</addr-line></aff><contrib-group><contrib contrib-type="editor"><name><surname>Mosley</surname><given-names>R. Lee</given-names></name><role>Editor</role><xref ref-type="aff" rid="edit1"></xref></contrib></contrib-group><aff id="edit1"><addr-line>University of Nebraska Medical Center, UNITED STATES</addr-line></aff><author-notes><fn fn-type="conflict" id="coi001"><p><bold>Competing Interests: </bold>The authors have declared that no competing interests exist. We have the following interests: This work was in part supported by Medos International Sàrl, a Johnson&Johnson company. Co-authors Blaise Lovisa and Yanik Tardy are employed by Medos International Sàrl, a Johnson&Johnson company. There are no patents, products in development or marketed products to declare. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.</p></fn><fn fn-type="con" id="contrib001"><p>Conceived and designed the experiments: AO HAL BL GW HvdB. Performed the experiments: AO BL JP. Analyzed the data: AO HAL BL GW HvdB YT. Wrote the paper: AO HAL.</p></fn><corresp id="cor001">* E-mail: <email>hilal.lashuel@epfl.ch</email> (HAL); <email>Abid.Oueslati@crchudequebec.ulaval.ca</email> (AO)</corresp></author-notes><pub-date pub-type="epub"><day>20</day><month>10</month><year>2015</year></pub-date><pub-date pub-type="collection"><year>2015</year></pub-date><volume>10</volume><issue>10</issue><elocation-id>e0140880</elocation-id><history><date date-type="received"><day>7</day><month>7</month><year>2015</year></date><date date-type="accepted"><day>1</day><month>10</month><year>2015</year></date></history><permissions><copyright-year>2015</copyright-year><copyright-holder>Oueslati et al</copyright-holder><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article distributed under the terms of the <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution License</ext-link>, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited</license-p></license></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="pone.0140880.pdf"></self-uri><abstract><p>Converging lines of evidence indicate that near-infrared light treatment, also known as photobiomodulation (PBM), may exert beneficial effects and protect against cellular toxicity and degeneration in several animal models of human pathologies, including neurodegenerative disorders. In the present study, we report that chronic PMB treatment mitigates dopaminergic loss induced by unilateral overexpression of human α-synuclein (α-syn) in the substantia nigra of an AAV-based rat genetic model of Parkinson’s disease (PD). In this model, daily exposure of both sides of the rat’s head to 808-nm near-infrared light for 28 consecutive days alleviated α-syn-induced motor impairment, as assessed using the cylinder test. This treatment also significantly reduced dopaminergic neuronal loss in the injected substantia nigra and preserved dopaminergic fibers in the ipsilateral striatum. These beneficial effects were sustained for at least 6 weeks after discontinuing the treatment. Together, our data point to PBM as a possible therapeutic strategy for the treatment of PD and other related synucleinopathies.</p></abstract><funding-group><funding-statement>This work was in part supported by Medos International Sàrl, a Johnson&Johnson company. The funder provided support in the form of salaries for authors [BL, YT], but did not have any additional role in the study design, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section. HAL, GW, HvdB and AO were supported by the Ecole Polytechnique Federal de Lausanne and JP and BL were supported by the Commission for Technology and Innovation (CTI). Additional supports were provided by the CTI projects 13758.1 and 14660.1, and the Swiss National Science Foundation (SNSF) projects N° 205320_147141 and CR32I3_159746.</funding-statement></funding-group><counts><fig-count count="6"></fig-count><table-count count="0"></table-count><page-count count="13"></page-count></counts><custom-meta-group><custom-meta id="data-availability"><meta-name>Data Availability</meta-name><meta-value>All relevant data are within the paper and its Supporting Information files.</meta-value></custom-meta></custom-meta-group></article-meta><notes><title>Data Availability</title><p>All relevant data are within the paper and its Supporting Information files.</p></notes></front></pmc><affiliations><list><country><li>Canada</li><li>Qatar</li><li>Suisse</li></country><region><li>Canton de Vaud</li></region><settlement><li>Lausanne</li></settlement></list><tree><country name="Suisse"><region name="Canton de Vaud"><name sortKey="Oueslati, Abid" sort="Oueslati, Abid" uniqKey="Oueslati A" first="Abid" last="Oueslati">Abid Oueslati</name></region><name sortKey="Lashuel, Hilal A" sort="Lashuel, Hilal A" uniqKey="Lashuel H" first="Hilal A." last="Lashuel">Hilal A. Lashuel</name><name sortKey="Lovisa, Blaise" sort="Lovisa, Blaise" uniqKey="Lovisa B" first="Blaise" last="Lovisa">Blaise Lovisa</name><name sortKey="Lovisa, Blaise" sort="Lovisa, Blaise" uniqKey="Lovisa B" first="Blaise" last="Lovisa">Blaise Lovisa</name><name sortKey="Perrin, John" sort="Perrin, John" uniqKey="Perrin J" first="John" last="Perrin">John Perrin</name><name sortKey="Tardy, Yanik" sort="Tardy, Yanik" uniqKey="Tardy Y" first="Yanik" last="Tardy">Yanik Tardy</name><name sortKey="Van Den Bergh, Hubert" sort="Van Den Bergh, Hubert" uniqKey="Van Den Bergh H" first="Hubert" last="Van Den Bergh">Hubert Van Den Bergh</name><name sortKey="Wagnieres, Georges" sort="Wagnieres, Georges" uniqKey="Wagnieres G" first="Georges" last="Wagnières">Georges Wagnières</name></country><country name="Canada"><noRegion><name sortKey="Oueslati, Abid" sort="Oueslati, Abid" uniqKey="Oueslati A" first="Abid" last="Oueslati">Abid Oueslati</name></noRegion></country><country name="Qatar"><noRegion><name sortKey="Lashuel, Hilal A" sort="Lashuel, Hilal A" uniqKey="Lashuel H" first="Hilal A." last="Lashuel">Hilal A. 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