IRC-082451, a novel multitargeting molecule, reduces L-DOPA-induced dyskinesias in MPTP Parkinsonian primates.
Identifieur interne : 000804 ( PubMed/Corpus ); précédent : 000803; suivant : 000805IRC-082451, a novel multitargeting molecule, reduces L-DOPA-induced dyskinesias in MPTP Parkinsonian primates.
Auteurs : Romina Aron Badin ; Brigitte Spinnewyn ; Marie-Claude Gaillard ; Caroline Jan ; Carole Malgorn ; Nadja Van Camp ; Frédéric Dollé ; Martine Guillermier ; Sabrina Boulet ; Anne Bertrand ; Marc Savasta ; Michel Auguet ; Emmanuel Brouillet ; Pierre-Etienne Chabrier ; Philippe HantrayeSource :
- PloS one [ 1932-6203 ] ; 2013.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Amantadine (pharmacology), Animals, Antioxidants (pharmacology), Antiparkinson Agents (pharmacology), Behavior, Animal, Chromatography, High Pressure Liquid, Cyclooxygenase Inhibitors (pharmacology), Disease Models, Animal, Dopamine Agents (pharmacology), Dyskinesias (metabolism), Immunohistochemistry, Levodopa (metabolism), Macaca fascicularis, Magnetic Resonance Imaging, Male, Neurons (drug effects), Oxidative Stress, Parkinson Disease (drug therapy), Positron-Emission Tomography, Thiazoles (pharmacology).
- MESH :
- chemical , metabolism : Levodopa.
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Amantadine, Antioxidants, Antiparkinson Agents, Cyclooxygenase Inhibitors, Dopamine Agents, Thiazoles.
- drug effects : Neurons.
- drug therapy : Parkinson Disease.
- metabolism : Dyskinesias.
- Animals, Behavior, Animal, Chromatography, High Pressure Liquid, Disease Models, Animal, Immunohistochemistry, Macaca fascicularis, Magnetic Resonance Imaging, Male, Oxidative Stress, Positron-Emission Tomography.
Abstract
The development of dyskinesias following chronic L-DOPA replacement therapy remains a major problem in the long-term treatment of Parkinson's disease. This study aimed at evaluating the effect of IRC-082451 (base of BN82451), a novel multitargeting hybrid molecule, on L-DOPA-induced dyskinesias (LIDs) and hypolocomotor activity in a non-human primate model of PD. IRC-082451 displays multiple properties: it inhibits neuronal excitotoxicity (sodium channel blocker), oxidative stress (antioxidant) and neuroinflammation (cyclooxygenase inhibitor) and is endowed with mitochondrial protective properties. Animals received daily MPTP injections until stably parkinsonian. A daily treatment with increasing doses of L-DOPA was administered to parkinsonian primates until the appearance of dyskinesias. Then, different treatment regimens and doses of IRC-082451 were tested and compared to the benchmark molecule amantadine. Primates were regularly filmed and videos were analyzed with specialized software. A novel approach combining the analysis of dyskinesias and locomotor activity was used to determine efficacy. This analysis yielded the quantification of the total distance travelled and the incidence of dyskinesias in 7 different body parts. A dose-dependent efficacy of IRC-082451 against dyskinesias was observed. The 5 mg/kg dose was best at attenuating the severity of fully established LIDs. Its effect was significantly different from that of amantadine since it increased spontaneous locomotor activity while reducing LIDs. This dose was effective both acutely and in a 5-day sub-chronic treatment. Moreover, positron emission tomography scans using radiolabelled dopamine demonstrated that there was no direct interference between treatment with IRC-082451 and dopamine metabolism in the brain. Finally, post-mortem analysis indicated that this reduction in dyskinesias was associated with changes in cFOS, FosB and ARC mRNA expression levels in the putamen. The data demonstrates the antidyskinetic efficacy of IRC-082451 in a primate model of PD with motor complications and opens the way to the clinical application of this treatment for the management of LIDs.
DOI: 10.1371/journal.pone.0052680
PubMed: 23300984
Links to Exploration step
pubmed:23300984Le document en format XML
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qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Amantadine</term><term>Antioxidants</term><term>Antiparkinson Agents</term><term>Cyclooxygenase Inhibitors</term><term>Dopamine Agents</term><term>Thiazoles</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dyskinesias</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Behavior, Animal</term><term>Chromatography, High Pressure Liquid</term><term>Disease Models, Animal</term><term>Immunohistochemistry</term><term>Macaca fascicularis</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Oxidative Stress</term><term>Positron-Emission Tomography</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The development of dyskinesias following chronic L-DOPA replacement therapy remains a major problem in the long-term treatment of Parkinson's disease. This study aimed at evaluating the effect of IRC-082451 (base of BN82451), a novel multitargeting hybrid molecule, on L-DOPA-induced dyskinesias (LIDs) and hypolocomotor activity in a non-human primate model of PD. IRC-082451 displays multiple properties: it inhibits neuronal excitotoxicity (sodium channel blocker), oxidative stress (antioxidant) and neuroinflammation (cyclooxygenase inhibitor) and is endowed with mitochondrial protective properties. Animals received daily MPTP injections until stably parkinsonian. A daily treatment with increasing doses of L-DOPA was administered to parkinsonian primates until the appearance of dyskinesias. Then, different treatment regimens and doses of IRC-082451 were tested and compared to the benchmark molecule amantadine. Primates were regularly filmed and videos were analyzed with specialized software. A novel approach combining the analysis of dyskinesias and locomotor activity was used to determine efficacy. This analysis yielded the quantification of the total distance travelled and the incidence of dyskinesias in 7 different body parts. A dose-dependent efficacy of IRC-082451 against dyskinesias was observed. The 5 mg/kg dose was best at attenuating the severity of fully established LIDs. Its effect was significantly different from that of amantadine since it increased spontaneous locomotor activity while reducing LIDs. This dose was effective both acutely and in a 5-day sub-chronic treatment. Moreover, positron emission tomography scans using radiolabelled dopamine demonstrated that there was no direct interference between treatment with IRC-082451 and dopamine metabolism in the brain. Finally, post-mortem analysis indicated that this reduction in dyskinesias was associated with changes in cFOS, FosB and ARC mRNA expression levels in the putamen. The data demonstrates the antidyskinetic efficacy of IRC-082451 in a primate model of PD with motor complications and opens the way to the clinical application of this treatment for the management of LIDs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23300984</PMID><DateCreated><Year>2013</Year><Month>01</Month><Day>09</Day></DateCreated><DateCompleted><Year>2013</Year><Month>08</Month><Day>20</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>1</Issue><PubDate><Year>2013</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>IRC-082451, a novel multitargeting molecule, reduces L-DOPA-induced dyskinesias in MPTP Parkinsonian primates.</ArticleTitle><Pagination><MedlinePgn>e52680</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0052680</ELocationID><Abstract><AbstractText>The development of dyskinesias following chronic L-DOPA replacement therapy remains a major problem in the long-term treatment of Parkinson's disease. This study aimed at evaluating the effect of IRC-082451 (base of BN82451), a novel multitargeting hybrid molecule, on L-DOPA-induced dyskinesias (LIDs) and hypolocomotor activity in a non-human primate model of PD. IRC-082451 displays multiple properties: it inhibits neuronal excitotoxicity (sodium channel blocker), oxidative stress (antioxidant) and neuroinflammation (cyclooxygenase inhibitor) and is endowed with mitochondrial protective properties. Animals received daily MPTP injections until stably parkinsonian. A daily treatment with increasing doses of L-DOPA was administered to parkinsonian primates until the appearance of dyskinesias. Then, different treatment regimens and doses of IRC-082451 were tested and compared to the benchmark molecule amantadine. Primates were regularly filmed and videos were analyzed with specialized software. A novel approach combining the analysis of dyskinesias and locomotor activity was used to determine efficacy. This analysis yielded the quantification of the total distance travelled and the incidence of dyskinesias in 7 different body parts. A dose-dependent efficacy of IRC-082451 against dyskinesias was observed. The 5 mg/kg dose was best at attenuating the severity of fully established LIDs. Its effect was significantly different from that of amantadine since it increased spontaneous locomotor activity while reducing LIDs. This dose was effective both acutely and in a 5-day sub-chronic treatment. Moreover, positron emission tomography scans using radiolabelled dopamine demonstrated that there was no direct interference between treatment with IRC-082451 and dopamine metabolism in the brain. Finally, post-mortem analysis indicated that this reduction in dyskinesias was associated with changes in cFOS, FosB and ARC mRNA expression levels in the putamen. The data demonstrates the antidyskinetic efficacy of IRC-082451 in a primate model of PD with motor complications and opens the way to the clinical application of this treatment for the management of LIDs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aron Badin</LastName><ForeName>Romina</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Molecular Imaging Research Center, Commissariat à l'Énergie Atomique, Fontenay-aux-Roses, France. romina.aron-badin@cea.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Spinnewyn</LastName><ForeName>Brigitte</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Gaillard</LastName><ForeName>Marie-Claude</ForeName><Initials>MC</Initials></Author><Author ValidYN="Y"><LastName>Jan</LastName><ForeName>Caroline</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Malgorn</LastName><ForeName>Carole</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Van Camp</LastName><ForeName>Nadja</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Dollé</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Guillermier</LastName><ForeName>Martine</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Boulet</LastName><ForeName>Sabrina</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Bertrand</LastName><ForeName>Anne</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Savasta</LastName><ForeName>Marc</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Auguet</LastName><ForeName>Michel</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Brouillet</LastName><ForeName>Emmanuel</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Chabrier</LastName><ForeName>Pierre-Etienne</ForeName><Initials>PE</Initials></Author><Author ValidYN="Y"><LastName>Hantraye</LastName><ForeName>Philippe</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>01</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016861">Cyclooxygenase Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C582899">IRC-082451</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013844">Thiazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>BF4C9Z1J53</RegistryNumber><NameOfSubstance UI="D000547">Amantadine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2000 Apr;47(4 Suppl 1):S60-8; discussion S68-9</RefSource><PMID 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MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3536787</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>07</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>11</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>1</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>1</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>8</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23300984</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0052680</ArticleId><ArticleId IdType="pii">PONE-D-12-23199</ArticleId><ArticleId IdType="pmc">PMC3536787</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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