Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an AAV-Based Rat Genetic Model of Parkinson's Disease.
Identifieur interne : 000383 ( PubMed/Corpus ); précédent : 000382; suivant : 000384Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an AAV-Based Rat Genetic Model of Parkinson's Disease.
Auteurs : Abid Oueslati ; Blaise Lovisa ; John Perrin ; Georges Wagnières ; Hubert Van Den Bergh ; Yanik Tardy ; Hilal A. LashuelSource :
- PloS one [ 1932-6203 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Corpus Striatum (metabolism), Corpus Striatum (pathology), Corpus Striatum (radiation effects), Disease Models, Animal, Dopaminergic Neurons (metabolism), Dopaminergic Neurons (pathology), Dopaminergic Neurons (radiation effects), Female, Low-Level Light Therapy, Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (radiotherapy), Rats, Rats, Sprague-Dawley, Substantia Nigra (metabolism), Substantia Nigra (pathology), Substantia Nigra (radiation effects).
- MESH :
- genetics : Parkinson Disease.
- metabolism : Corpus Striatum, Dopaminergic Neurons, Parkinson Disease, Substantia Nigra.
- pathology : Corpus Striatum, Dopaminergic Neurons, Parkinson Disease, Substantia Nigra.
- radiation effects : Corpus Striatum, Dopaminergic Neurons, Substantia Nigra.
- radiotherapy : Parkinson Disease.
- Animals, Disease Models, Animal, Female, Low-Level Light Therapy, Rats, Rats, Sprague-Dawley.
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.
DOI: 10.1371/journal.pone.0140880
PubMed: 26484876
Links to Exploration step
pubmed:26484876Le document en format XML
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Lashuel</name><affiliation><nlm:affiliation>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland; Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. 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Lashuel</name><affiliation><nlm:affiliation>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland; Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. Box 5825, Doha, Qatar.</nlm:affiliation></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Corpus Striatum (radiation effects)</term><term>Disease Models, Animal</term><term>Dopaminergic Neurons (metabolism)</term><term>Dopaminergic Neurons (pathology)</term><term>Dopaminergic Neurons (radiation effects)</term><term>Female</term><term>Low-Level Light Therapy</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (radiotherapy)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Substantia Nigra (radiation effects)</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Dopaminergic Neurons</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Dopaminergic Neurons</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Corpus Striatum</term><term>Dopaminergic Neurons</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="radiotherapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Low-Level Light Therapy</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26484876</PMID><DateCreated><Year>2015</Year><Month>10</Month><Day>21</Day></DateCreated><DateCompleted><Year>2016</Year><Month>06</Month><Day>07</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>10</Issue><PubDate><Year>2015</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an AAV-Based Rat Genetic Model of Parkinson's Disease.</ArticleTitle><Pagination><MedlinePgn>e0140880</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0140880</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Oueslati</LastName><ForeName>Abid</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland; Centre de Recherche du Centre Hospitalier de Québec, Axe Neuroscience et Département de Médecine Moléculaire de l'Université Laval, Québec, G1V4G2, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lovisa</LastName><ForeName>Blaise</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Institute of Chemical Sciences and Engineering, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland; Medos International Sàrl, a Johnson&Johnson company, Chemin Blanc 38, CH-2400, Le Locle, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perrin</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wagnières</LastName><ForeName>Georges</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Institute of Chemical Sciences and Engineering, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van den Bergh</LastName><ForeName>Hubert</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Institute of Chemical Sciences and Engineering, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tardy</LastName><ForeName>Yanik</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Medos International Sàrl, a Johnson&Johnson company, Chemin Blanc 38, CH-2400, Le Locle, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lashuel</LastName><ForeName>Hilal A</ForeName><Initials>HA</Initials><AffiliationInfo><Affiliation>Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Swiss Federal Institute of Technology (EPFL), CH-1015, Lausanne, Switzerland; Qatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, P.O. 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