An evaluation of istradefylline treatment on Parkinsonian motor and cognitive deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque models.
Identifieur interne : 000068 ( PubMed/Corpus ); précédent : 000067; suivant : 000069An evaluation of istradefylline treatment on Parkinsonian motor and cognitive deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque models.
Auteurs : Wai Kin D. Ko ; Sandrine M. Camus ; Qin Li ; Jianzhong Yang ; Steve Mcguire ; Elsa Y. Pioli ; Erwan BezardSource :
- Neuropharmacology [ 1873-7064 ] ; 2016.
Abstract
Istradefylline (KW-6002), an adenosine A2A receptor antagonist, is used adjunct with optimal doses of L-3,4-dihydroxyphenylalanine (l-DOPA) to extend on-time in Parkinson's disease (PD) patients experiencing motor fluctuations. Clinical application of istradefylline for the management of other l-DOPA-induced complications, both motor and non-motor related (i.e. dyskinesia and cognitive impairments), remains to be determined. In this study, acute effects of istradefylline (60-100 mg/kg) alone, or with optimal and sub-optimal doses of l-DOPA, were evaluated in two monkey models of PD (i) the gold-standard 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque model of parkinsonian and dyskinetic motor symptoms and (ii) the chronic low dose (CLD) MPTP-treated macaque model of cognitive (working memory and attentional) deficits. Behavioural analyses in l-DOPA-primed MPTP-treated macaques showed that istradefylline alone specifically alleviated postural deficits. When combined with an optimal l-DOPA treatment dose, istradefylline increased on-time, enhanced therapeutic effects on bradykinesia and locomotion, but exacerbated dyskinesia. Istradefylline treatment at specific doses with sub-optimal l-DOPA specifically alleviated bradykinesia. Cognitive assessments in CLD MPTP-treated macaques showed that the attentional and working memory deficits caused by l-DOPA were lowered after istradefylline administration. Taken together, these data support a broader clinical use of istradefylline as an adjunct treatment in PD, where specific treatment combinations can be utilised to manage various l-DOPA-induced complications, which importantly, maintain a desired anti-parkinsonian response.
DOI: 10.1016/j.neuropharm.2016.07.012
PubMed: 27424102
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">An evaluation of istradefylline treatment on Parkinsonian motor and cognitive deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque models.</title><author><name sortKey="Ko, Wai Kin D" sort="Ko, Wai Kin D" uniqKey="Ko W" first="Wai Kin D" last="Ko">Wai Kin D. Ko</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom. Electronic address: d.ko@motac.com.</nlm:affiliation></affiliation></author><author><name sortKey="Camus, Sandrine M" sort="Camus, Sandrine M" uniqKey="Camus S" first="Sandrine M" last="Camus">Sandrine M. Camus</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jianzhong" sort="Yang, Jianzhong" uniqKey="Yang J" first="Jianzhong" last="Yang">Jianzhong Yang</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Mcguire, Steve" sort="Mcguire, Steve" uniqKey="Mcguire S" first="Steve" last="Mcguire">Steve Mcguire</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Pioli, Elsa Y" sort="Pioli, Elsa Y" uniqKey="Pioli E" first="Elsa Y" last="Pioli">Elsa Y. Pioli</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom; Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27424102</idno><idno type="pmid">27424102</idno><idno type="doi">10.1016/j.neuropharm.2016.07.012</idno><idno type="wicri:Area/PubMed/Corpus">000068</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000068</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">An evaluation of istradefylline treatment on Parkinsonian motor and cognitive deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque models.</title><author><name sortKey="Ko, Wai Kin D" sort="Ko, Wai Kin D" uniqKey="Ko W" first="Wai Kin D" last="Ko">Wai Kin D. Ko</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom. Electronic address: d.ko@motac.com.</nlm:affiliation></affiliation></author><author><name sortKey="Camus, Sandrine M" sort="Camus, Sandrine M" uniqKey="Camus S" first="Sandrine M" last="Camus">Sandrine M. Camus</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jianzhong" sort="Yang, Jianzhong" uniqKey="Yang J" first="Jianzhong" last="Yang">Jianzhong Yang</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Mcguire, Steve" sort="Mcguire, Steve" uniqKey="Mcguire S" first="Steve" last="Mcguire">Steve Mcguire</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Pioli, Elsa Y" sort="Pioli, Elsa Y" uniqKey="Pioli E" first="Elsa Y" last="Pioli">Elsa Y. Pioli</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation><nlm:affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom; Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Neuropharmacology</title><idno type="eISSN">1873-7064</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Istradefylline (KW-6002), an adenosine A2A receptor antagonist, is used adjunct with optimal doses of L-3,4-dihydroxyphenylalanine (l-DOPA) to extend on-time in Parkinson's disease (PD) patients experiencing motor fluctuations. Clinical application of istradefylline for the management of other l-DOPA-induced complications, both motor and non-motor related (i.e. dyskinesia and cognitive impairments), remains to be determined. In this study, acute effects of istradefylline (60-100 mg/kg) alone, or with optimal and sub-optimal doses of l-DOPA, were evaluated in two monkey models of PD (i) the gold-standard 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque model of parkinsonian and dyskinetic motor symptoms and (ii) the chronic low dose (CLD) MPTP-treated macaque model of cognitive (working memory and attentional) deficits. Behavioural analyses in l-DOPA-primed MPTP-treated macaques showed that istradefylline alone specifically alleviated postural deficits. When combined with an optimal l-DOPA treatment dose, istradefylline increased on-time, enhanced therapeutic effects on bradykinesia and locomotion, but exacerbated dyskinesia. Istradefylline treatment at specific doses with sub-optimal l-DOPA specifically alleviated bradykinesia. Cognitive assessments in CLD MPTP-treated macaques showed that the attentional and working memory deficits caused by l-DOPA were lowered after istradefylline administration. Taken together, these data support a broader clinical use of istradefylline as an adjunct treatment in PD, where specific treatment combinations can be utilised to manage various l-DOPA-induced complications, which importantly, maintain a desired anti-parkinsonian response.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">27424102</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>19</Day></DateCreated><DateRevised><Year>2016</Year><Month>09</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-7064</ISSN><JournalIssue CitedMedium="Internet"><Volume>110</Volume><Issue>Pt A</Issue><PubDate><Year>2016</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Neuropharmacology</Title><ISOAbbreviation>Neuropharmacology</ISOAbbreviation></Journal><ArticleTitle>An evaluation of istradefylline treatment on Parkinsonian motor and cognitive deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque models.</ArticleTitle><Pagination><MedlinePgn>48-58</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neuropharm.2016.07.012</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0028-3908(16)30298-2</ELocationID><Abstract><AbstractText>Istradefylline (KW-6002), an adenosine A2A receptor antagonist, is used adjunct with optimal doses of L-3,4-dihydroxyphenylalanine (l-DOPA) to extend on-time in Parkinson's disease (PD) patients experiencing motor fluctuations. Clinical application of istradefylline for the management of other l-DOPA-induced complications, both motor and non-motor related (i.e. dyskinesia and cognitive impairments), remains to be determined. In this study, acute effects of istradefylline (60-100 mg/kg) alone, or with optimal and sub-optimal doses of l-DOPA, were evaluated in two monkey models of PD (i) the gold-standard 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaque model of parkinsonian and dyskinetic motor symptoms and (ii) the chronic low dose (CLD) MPTP-treated macaque model of cognitive (working memory and attentional) deficits. Behavioural analyses in l-DOPA-primed MPTP-treated macaques showed that istradefylline alone specifically alleviated postural deficits. When combined with an optimal l-DOPA treatment dose, istradefylline increased on-time, enhanced therapeutic effects on bradykinesia and locomotion, but exacerbated dyskinesia. Istradefylline treatment at specific doses with sub-optimal l-DOPA specifically alleviated bradykinesia. Cognitive assessments in CLD MPTP-treated macaques showed that the attentional and working memory deficits caused by l-DOPA were lowered after istradefylline administration. Taken together, these data support a broader clinical use of istradefylline as an adjunct treatment in PD, where specific treatment combinations can be utilised to manage various l-DOPA-induced complications, which importantly, maintain a desired anti-parkinsonian response.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ko</LastName><ForeName>Wai Kin D</ForeName><Initials>WK</Initials><AffiliationInfo><Affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom. Electronic address: d.ko@motac.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Camus</LastName><ForeName>Sandrine M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qin</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Jianzhong</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McGuire</LastName><ForeName>Steve</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pioli</LastName><ForeName>Elsa Y</ForeName><Initials>EY</Initials><AffiliationInfo><Affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>Erwan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Motac Neuroscience Ltd, Manchester, United Kingdom; Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>07</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Neuropharmacology</MedlineTA><NlmUniqueID>0236217</NlmUniqueID><ISSNLinking>0028-3908</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cognition</Keyword><Keyword MajorTopicYN="N">Istradefylline</Keyword><Keyword MajorTopicYN="N">KW-6002</Keyword><Keyword MajorTopicYN="N">MPTP</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">l-DOPA-induced dyskinesia</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>02</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>07</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>07</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>7</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>7</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>7</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27424102</ArticleId><ArticleId IdType="pii">S0028-3908(16)30298-2</ArticleId><ArticleId IdType="doi">10.1016/j.neuropharm.2016.07.012</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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