Modeling dyskinesia in animal models of Parkinson disease : ANIMAL MODELS OF PARKINSON'S DISEASE
Identifieur interne : 000014 ( PascalFrancis/Checkpoint ); précédent : 000013; suivant : 000015Modeling dyskinesia in animal models of Parkinson disease : ANIMAL MODELS OF PARKINSON'S DISEASE
Auteurs : Nicolas Morin [Canada] ; Vincent A. Jourdain ; Thérèse Di PaoloSource :
- Experimental neurology : (Print) [ 0014-4886 ] ; 2014.
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Abstract
The treatment of motor symptoms of Parkinson disease (PD) with the dopamine (DA) precursor, L-3,4-dihydroxyphenylalanine (L-DOPA) introduced 50 years ago still remains a very effective medication. However, involuntary movements termed L-DOPA-induced dyskinesias (LID) appear in the vast majority of PD patients after chronic treatment and may become disabling. Once they appeared, the first dose after a several-weeks drug holiday will trigger them again, showing that L-DOPA has permanently or persistently modified the brain response to DA. LID are very difficult to manage and no drug is yet approved for dyskinesias, aside from a modest benefit with amantadine. New drugs are needed for PD to alleviate parkinsonian symptoms without inducing dyskinesias. Hence, animal models have been developed to seek the mechanisms involved in LID and new drug targets. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was discovered as a contamination of a derivative of heroin taken by drug users and produced similar motor symptoms as idiopathic PD. Since then, MPTP is used extensively to model PD and LID in non-human primates and mice in addition to the classical PD model in rats with a 6-hydroxydopamine (6-OHDA) lesion. This article reviews rodent and non-human primate models of PD that reproduce motor complications induced by DA replacement therapy. Moreover, key biochemical changes in the brain of post-mortem PD patients with LID will be compared to those observed in animal models. Finally, the translational usefulness of drugs found to treat LID in animal models will be compared to their clinical activities.
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Jourdain</name></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">14-0182393</idno><date when="2014">2014</date><idno type="stanalyst">PASCAL 14-0182393 INIST</idno><idno type="RBID">Pascal:14-0182393</idno><idno type="wicri:Area/PascalFrancis/Corpus">000018</idno><idno type="wicri:Area/PascalFrancis/Curation">000C00</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000014</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000014</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Modeling dyskinesia in animal models of Parkinson disease : ANIMAL MODELS OF PARKINSON'S DISEASE</title><author><name sortKey="Morin, Nicolas" sort="Morin, Nicolas" uniqKey="Morin N" first="Nicolas" last="Morin">Nicolas Morin</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuroscience Research Unit, Centre de recherche du CHU de Québec</s1><s2>Quebec (QC)</s2><s3>CAN</s3></inist:fA14><country>Canada</country><wicri:noRegion>Quebec (QC)</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1><s2>Quebec (QC)</s2><s3>CAN</s3></inist:fA14><country>Canada</country><wicri:noRegion>Quebec (QC)</wicri:noRegion></affiliation></author><author><name sortKey="Jourdain, Vincent A" sort="Jourdain, Vincent A" uniqKey="Jourdain V" first="Vincent A." last="Jourdain">Vincent A. Jourdain</name></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name></author></analytic><series><title level="j" type="main">Experimental neurology : (Print)</title><title level="j" type="abbreviated">Exp. neurol. : (Print)</title><idno type="ISSN">0014-4886</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Experimental neurology : (Print)</title><title level="j" type="abbreviated">Exp. neurol. : (Print)</title><idno type="ISSN">0014-4886</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abnormal movement</term><term>Animal</term><term>Animal model</term><term>Complication</term><term>Dyskinesia</term><term>Involuntary movement</term><term>Levodopa</term><term>Modeling</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Primates</term><term>Rodentia</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dyskinésie</term><term>Maladie de Parkinson</term><term>Mouvement involontaire</term><term>Pathologie du système nerveux</term><term>Modélisation</term><term>Modèle animal</term><term>Lévodopa</term><term>Primates</term><term>Rodentia</term><term>Animal</term><term>Mouvement anormal</term><term>Complication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The treatment of motor symptoms of Parkinson disease (PD) with the dopamine (DA) precursor, L-3,4-dihydroxyphenylalanine (L-DOPA) introduced 50 years ago still remains a very effective medication. However, involuntary movements termed L-DOPA-induced dyskinesias (LID) appear in the vast majority of PD patients after chronic treatment and may become disabling. Once they appeared, the first dose after a several-weeks drug holiday will trigger them again, showing that L-DOPA has permanently or persistently modified the brain response to DA. LID are very difficult to manage and no drug is yet approved for dyskinesias, aside from a modest benefit with amantadine. New drugs are needed for PD to alleviate parkinsonian symptoms without inducing dyskinesias. Hence, animal models have been developed to seek the mechanisms involved in LID and new drug targets. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was discovered as a contamination of a derivative of heroin taken by drug users and produced similar motor symptoms as idiopathic PD. Since then, MPTP is used extensively to model PD and LID in non-human primates and mice in addition to the classical PD model in rats with a 6-hydroxydopamine (6-OHDA) lesion. This article reviews rodent and non-human primate models of PD that reproduce motor complications induced by DA replacement therapy. Moreover, key biochemical changes in the brain of post-mortem PD patients with LID will be compared to those observed in animal models. 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Jourdain</name></noCountry><country name="Canada"><noRegion><name sortKey="Morin, Nicolas" sort="Morin, Nicolas" uniqKey="Morin N" first="Nicolas" last="Morin">Nicolas Morin</name></noRegion><name sortKey="Morin, Nicolas" sort="Morin, Nicolas" uniqKey="Morin N" first="Nicolas" last="Morin">Nicolas Morin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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