Levodopa/dopamine replacement strategies in Parkinson's disease—Future directions
Identifieur interne : 003362 ( Main/Merge ); précédent : 003361; suivant : 003363Levodopa/dopamine replacement strategies in Parkinson's disease—Future directions
Auteurs : C. Warren Olanow [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2008.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (therapeutic use), Catechol O-Methyltransferase Inhibitors, Corpus Striatum (drug effects), Corpus Striatum (physiopathology), Disease Models, Animal, Dopamine (secretion), Dopamine (therapeutic use), Drug Administration Schedule, Enzyme Inhibitors (therapeutic use), Humans, Levodopa (administration & dosage), Levodopa (therapeutic use), Neurons (drug effects), Neurons (physiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson's disease, Substantia Nigra (drug effects), Substantia Nigra (physiopathology), levodopa, motor complications.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Levodopa.
- chemical , secretion : Dopamine.
- chemical , therapeutic use : Antiparkinson Agents, Dopamine, Enzyme Inhibitors, Levodopa.
- drug effects : Corpus Striatum, Neurons, Substantia Nigra.
- drug therapy : Parkinson Disease.
- physiology : Neurons.
- physiopathology : Corpus Striatum, Parkinson Disease, Substantia Nigra.
- Animals, Catechol O-Methyltransferase Inhibitors, Disease Models, Animal, Drug Administration Schedule, Humans.
Abstract
After 40 years, levodopa remains the most effective therapy for the treatment of PD. However, long‐term therapy is complicated by motor fluctuations and dyskinesia that can represent a source of significant disability for some patients. Other medical therapies that are currently available for the treatment of PD primarily represent an attempt to prevent or treat motor complications. Surgical therapies improve motor complications in appropriate candidates, but do not provide antiparkinsonian benefits that are superior to levodopa, and are themselves associated with potentially serious side effects. Increasing information suggests that levodopa‐induced motor complications relate to pulsatile, nonphysiologic dopamine replacement. A therapeutic strategy that could deliver levodopa/dopamine to the brain in a more continuous and physiologic manner might be expected to provide all of the benefits of standard levodopa with reduced motor complications. Such a levodopa formulation might replace all current dopaminergic antiparkinsonian medications and avoid the need for surgery in most PD patients. However, problems of continuous dopaminergic stimulation must be addressed and avoided, and the issue of nondopaminergic features remains to be addressed. © 2008 Movement Disorder Society
Url:
DOI: 10.1002/mds.22061
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Warren" last="Olanow">C. 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><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 Neuroscience, Mount Sinai School of Medicine, New York</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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However, long‐term therapy is complicated by motor fluctuations and dyskinesia that can represent a source of significant disability for some patients. Other medical therapies that are currently available for the treatment of PD primarily represent an attempt to prevent or treat motor complications. Surgical therapies improve motor complications in appropriate candidates, but do not provide antiparkinsonian benefits that are superior to levodopa, and are themselves associated with potentially serious side effects. Increasing information suggests that levodopa‐induced motor complications relate to pulsatile, nonphysiologic dopamine replacement. A therapeutic strategy that could deliver levodopa/dopamine to the brain in a more continuous and physiologic manner might be expected to provide all of the benefits of standard levodopa with reduced motor complications. Such a levodopa formulation might replace all current dopaminergic antiparkinsonian medications and avoid the need for surgery in most PD patients. However, problems of continuous dopaminergic stimulation must be addressed and avoided, and the issue of nondopaminergic features remains to be addressed. © 2008 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.22061"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Levodopa/dopamine replacement strategies in Parkinson's disease—Future directions</title><author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C. Warren" last="Olanow">C. Warren Olanow</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DE47B16EADA7DA2584E4EF83B378C9AA40D6E31B</idno><date when="2008" year="2008">2008</date><idno type="doi">10.1002/mds.22061</idno><idno type="url">https://api.istex.fr/document/DE47B16EADA7DA2584E4EF83B378C9AA40D6E31B/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000937</idno><idno type="wicri:Area/Istex/Curation">000937</idno><idno type="wicri:Area/Istex/Checkpoint">001340</idno><idno type="wicri:doubleKey">0885-3185:2008:Olanow C:levodopa:dopamine:replacement</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Levodopa/dopamine replacement strategies in Parkinson's disease—Future directions</title><author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C. Warren" last="Olanow">C. 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><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 Neuroscience, Mount Sinai School of Medicine, New York</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008">2008</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">S3</biblScope><biblScope unit="supplement">S3</biblScope><biblScope unit="page" from="S613">S613</biblScope><biblScope unit="page" to="S622">S622</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">DE47B16EADA7DA2584E4EF83B378C9AA40D6E31B</idno><idno type="DOI">10.1002/mds.22061</idno><idno type="ArticleID">MDS22061</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>levodopa</term><term>motor complications</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">After 40 years, levodopa remains the most effective therapy for the treatment of PD. However, long‐term therapy is complicated by motor fluctuations and dyskinesia that can represent a source of significant disability for some patients. Other medical therapies that are currently available for the treatment of PD primarily represent an attempt to prevent or treat motor complications. Surgical therapies improve motor complications in appropriate candidates, but do not provide antiparkinsonian benefits that are superior to levodopa, and are themselves associated with potentially serious side effects. Increasing information suggests that levodopa‐induced motor complications relate to pulsatile, nonphysiologic dopamine replacement. A therapeutic strategy that could deliver levodopa/dopamine to the brain in a more continuous and physiologic manner might be expected to provide all of the benefits of standard levodopa with reduced motor complications. Such a levodopa formulation might replace all current dopaminergic antiparkinsonian medications and avoid the need for surgery in most PD patients. However, problems of continuous dopaminergic stimulation must be addressed and avoided, and the issue of nondopaminergic features remains to be addressed. © 2008 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Levodopa/dopamine replacement strategies in Parkinson's disease--future directions.</title><author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C Warren" last="Olanow">C Warren Olanow</name><affiliation wicri:level="2"><nlm:affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA. warren.olanow@mssm.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mount Sinai School of Medicine, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="doi">10.1002/mds.22061</idno><idno type="RBID">pubmed:18781663</idno><idno type="pmid">18781663</idno><idno type="wicri:Area/PubMed/Corpus">002061</idno><idno type="wicri:Area/PubMed/Curation">002061</idno><idno type="wicri:Area/PubMed/Checkpoint">002234</idno><idno type="wicri:Area/Ncbi/Merge">002302</idno><idno type="wicri:Area/Ncbi/Curation">002302</idno><idno type="wicri:Area/Ncbi/Checkpoint">002302</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Levodopa/dopamine replacement strategies in Parkinson's disease--future directions.</title><author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C Warren" last="Olanow">C Warren Olanow</name><affiliation wicri:level="2"><nlm:affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA. warren.olanow@mssm.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mount Sinai School of Medicine, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Catechol O-Methyltransferase Inhibitors</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (physiopathology)</term><term>Disease Models, Animal</term><term>Dopamine (secretion)</term><term>Dopamine (therapeutic use)</term><term>Drug Administration Schedule</term><term>Enzyme Inhibitors (therapeutic use)</term><term>Humans</term><term>Levodopa (administration & dosage)</term><term>Levodopa (therapeutic use)</term><term>Neurons (drug effects)</term><term>Neurons (physiology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="secretion" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine</term><term>Enzyme Inhibitors</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Corpus Striatum</term><term>Neurons</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Catechol O-Methyltransferase Inhibitors</term><term>Disease Models, Animal</term><term>Drug Administration Schedule</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">After 40 years, levodopa remains the most effective therapy for the treatment of PD. However, long-term therapy is complicated by motor fluctuations and dyskinesia that can represent a source of significant disability for some patients. Other medical therapies that are currently available for the treatment of PD primarily represent an attempt to prevent or treat motor complications. Surgical therapies improve motor complications in appropriate candidates, but do not provide antiparkinsonian benefits that are superior to levodopa, and are themselves associated with potentially serious side effects. Increasing information suggests that levodopa-induced motor complications relate to pulsatile, nonphysiologic dopamine replacement. A therapeutic strategy that could deliver levodopa/dopamine to the brain in a more continuous and physiologic manner might be expected to provide all of the benefits of standard levodopa with reduced motor complications. Such a levodopa formulation might replace all current dopaminergic antiparkinsonian medications and avoid the need for surgery in most PD patients. However, problems of continuous dopaminergic stimulation must be addressed and avoided, and the issue of nondopaminergic features remains to be addressed.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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