The dopamine transporter: Importance in Parkinson's disease
Identifieur interne : 001566 ( Main/Exploration ); précédent : 001565; suivant : 001567The dopamine transporter: Importance in Parkinson's disease
Auteurs : John G. Nutt [États-Unis] ; Julie H. Carter [États-Unis] ; Gary J. Sexton [États-Unis]Source :
- Annals of Neurology [ 0364-5134 ] ; 2004-06.
Abstract
The dopamine transporter (DAT) may be the single most important determinant of extracellular dopamine concentrations. The importance of DAT in Parkinson's disease (PD) in which DAT may be reduced by 50 to 70% is unclear. We have examined the effects of methylphenidate (MPD), an inhibitor of DAT, administered alone or with levodopa, on parkinsonism measured with tapping and walking speeds, dyskinesia, subjective effects, and vital signs. MPD in oral doses of up to 0.4mg/kg was well tolerated. Administered alone, MPD produced no objective improvement of parkinsonism. MPD, 0.4mg/kg orally, coadministered with 2‐hour levodopa infusions at 0.5 or 1.0mg/kg/hr increased the percentage of patients responding to the 0.5mg/kg/hr dose and prolonged the response to levodopa infusions as measured by tapping and walking speeds. Dyskinesia was prolonged in proportion to the increase in antiparkinson actions but severity was not increased. MPD decreased the hypotensive response to levodopa. In conclusion, MPD appeared to have no effect given alone but potentiated the effects of levodopa, particularly doses at threshold for clinical effects. These observations indicate that the residual DAT is functional in PD and is a potential target for symptomatic therapy of PD.
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DOI: 10.1002/ana.20089
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Nutt</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Department of Neurology, Oregon Health and Science University, Portland</wicri:cityArea></affiliation><affiliation><wicri:noCountry code="subField">Education and Clinical Center (PADRECC)</wicri:noCountry></affiliation></author><author><name sortKey="Carter, Julie H" sort="Carter, Julie H" uniqKey="Carter J" first="Julie H." last="Carter">Julie H. Carter</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Department of Neurology, Oregon Health and Science University, Portland</wicri:cityArea></affiliation></author><author><name sortKey="Sexton, Gary J" sort="Sexton, Gary J" uniqKey="Sexton G" first="Gary J." last="Sexton">Gary J. Sexton</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>General Clinical Research Center, Oregon Health and Science University, Portland</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-06">2004-06</date><biblScope unit="volume">55</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="766">766</biblScope><biblScope unit="page" to="773">773</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">F6EFBFA3ADD68C40DE57C09253FC370B22C749F1</idno><idno type="DOI">10.1002/ana.20089</idno><idno type="ArticleID">ANA20089</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The dopamine transporter (DAT) may be the single most important determinant of extracellular dopamine concentrations. The importance of DAT in Parkinson's disease (PD) in which DAT may be reduced by 50 to 70% is unclear. We have examined the effects of methylphenidate (MPD), an inhibitor of DAT, administered alone or with levodopa, on parkinsonism measured with tapping and walking speeds, dyskinesia, subjective effects, and vital signs. MPD in oral doses of up to 0.4mg/kg was well tolerated. Administered alone, MPD produced no objective improvement of parkinsonism. MPD, 0.4mg/kg orally, coadministered with 2‐hour levodopa infusions at 0.5 or 1.0mg/kg/hr increased the percentage of patients responding to the 0.5mg/kg/hr dose and prolonged the response to levodopa infusions as measured by tapping and walking speeds. Dyskinesia was prolonged in proportion to the increase in antiparkinson actions but severity was not increased. MPD decreased the hypotensive response to levodopa. In conclusion, MPD appeared to have no effect given alone but potentiated the effects of levodopa, particularly doses at threshold for clinical effects. These observations indicate that the residual DAT is functional in PD and is a potential target for symptomatic therapy of PD.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Oregon</li></region></list><tree><country name="États-Unis"><region name="Oregon"><name sortKey="Nutt, John G" sort="Nutt, John G" uniqKey="Nutt J" first="John G." last="Nutt">John G. Nutt</name></region><name sortKey="Carter, Julie H" sort="Carter, Julie H" uniqKey="Carter J" first="Julie H." last="Carter">Julie H. Carter</name><name sortKey="Sexton, Gary J" sort="Sexton, Gary J" uniqKey="Sexton G" first="Gary J." last="Sexton">Gary J. Sexton</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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