Dopamine agonists and neuroprotection in parkinson's disease
Identifieur interne : 001F05 ( Main/Exploration ); précédent : 001F04; suivant : 001F06Dopamine agonists and neuroprotection in parkinson's disease
Auteurs : C. Warren Olanow [États-Unis] ; Peter Jenner [Royaume-Uni] ; David Brooks [Royaume-Uni]Source :
- Annals of Neurology [ 0364-5134 ] ; 1998-09.
Abstract
There is increasing interest in the potential of dopamine agonists to provide a neuroprotective effect and to alter the natural course of levodopa‐treated Parkinson's disease (PD). Theoretically, such a protective effect might derive from (a) a levodopa sparing effect, (b) stimulation dopamine autoreceptors resulting in decreased dopamine synthesis, release, and turnover, (c) direct anti‐oxidant effects, and (d) restoration of dopaminergic tone to the dopamine‐denervated brain so as to restore inhibition to the subthalamic nucleus and thereby diminish STN‐mediated excitotoxicity. Preclinical studies have demonstrated that dopamine agonists reduce dopamine formation in comparison to levodopa, protect cultured dopaminergic neurons from a variety of toxins including levodopa, and protect dopaminergic neurons from toxins and age‐related degeneration in some rodent models of parkinsonism. Based on these findings, several clinical trials have been initiated in patients with early PD to test the effect of dopamine agonists on clinical and neuroimaging markers of disease progression.
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DOI: 10.1002/ana.410440725
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Warren Olanow</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Department of Neurology, Mount Sinai School of Medicine, New York</wicri:cityArea></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Neurodegenerative Diseases Research Centre, King's College London</wicri:regionArea><wicri:noRegion>King's College London</wicri:noRegion></affiliation></author><author><name sortKey="Brooks, David" sort="Brooks, David" uniqKey="Brooks D" first="David" last="Brooks">David Brooks</name><affiliation wicri:level="3"><country xml:lang="fr" wicri:curation="lc">Royaume-Uni</country><wicri:regionArea>MRC Cyclotron Unit, Hammersmith Hospital, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</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="1998-09">1998-09</date><biblScope unit="volume">44</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="supplement">1</biblScope><biblScope unit="page" from="S167">S167</biblScope><biblScope unit="page" to="S174">S174</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">10A440F747EA250B45D747B68EFCCE7BFC4AA026</idno><idno type="DOI">10.1002/ana.410440725</idno><idno type="ArticleID">ANA410440725</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">There is increasing interest in the potential of dopamine agonists to provide a neuroprotective effect and to alter the natural course of levodopa‐treated Parkinson's disease (PD). Theoretically, such a protective effect might derive from (a) a levodopa sparing effect, (b) stimulation dopamine autoreceptors resulting in decreased dopamine synthesis, release, and turnover, (c) direct anti‐oxidant effects, and (d) restoration of dopaminergic tone to the dopamine‐denervated brain so as to restore inhibition to the subthalamic nucleus and thereby diminish STN‐mediated excitotoxicity. Preclinical studies have demonstrated that dopamine agonists reduce dopamine formation in comparison to levodopa, protect cultured dopaminergic neurons from a variety of toxins including levodopa, and protect dopaminergic neurons from toxins and age‐related degeneration in some rodent models of parkinsonism. Based on these findings, several clinical trials have been initiated in patients with early PD to test the effect of dopamine agonists on clinical and neuroimaging markers of disease progression.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Grand Londres</li><li>État de New York</li></region><settlement><li>Londres</li></settlement></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="C Warren Olanow" sort="C Warren Olanow" uniqKey="C Warren Olanow" last="C. Warren Olanow">C. Warren Olanow</name></region></country><country name="Royaume-Uni"><noRegion><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name></noRegion><name sortKey="Brooks, David" sort="Brooks, David" uniqKey="Brooks D" first="David" last="Brooks">David Brooks</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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