Neuroprotective therapy in Parkinson's disease and motor complications: a search for a pathogenesis-targeted, disease-modifying strategy.
Identifieur interne : 003077 ( PubMed/Curation ); précédent : 003076; suivant : 003078Neuroprotective therapy in Parkinson's disease and motor complications: a search for a pathogenesis-targeted, disease-modifying strategy.
Auteurs : C Warren Olanow [États-Unis] ; Joseph JankovicSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Antiparkinson Agents (adverse effects), Antiparkinson Agents (therapeutic use), Coenzymes, Cyclooxygenase 1, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors (therapeutic use), Dose-Response Relationship, Drug, Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (prevention & control), Humans, Indans (therapeutic use), Levodopa (adverse effects), Levodopa (therapeutic use), Membrane Proteins, N-Methylaspartate (antagonists & inhibitors), Neuroprotective Agents (therapeutic use), Parkinson Disease (drug therapy), Prostaglandin-Endoperoxide Synthases (metabolism), Ubiquinone (analogs & derivatives), Ubiquinone (therapeutic use), Vitamin E (therapeutic use).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , analogs & derivatives : Ubiquinone.
- chemical , antagonists & inhibitors : N-Methylaspartate.
- chemical , metabolism : Prostaglandin-Endoperoxide Synthases.
- chemical , therapeutic use : Anti-Inflammatory Agents, Non-Steroidal, Antiparkinson Agents, Cyclooxygenase Inhibitors, Indans, Levodopa, Neuroprotective Agents, Ubiquinone, Vitamin E.
- chemical : Coenzymes, Cyclooxygenase 1, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Membrane Proteins.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- prevention & control : Dyskinesia, Drug-Induced.
- Dose-Response Relationship, Drug, Humans.
Abstract
The introduction of levodopa in the late 1960s represented a landmark in the therapy of Parkinson's disease (PD). However, motor complications of chronic levodopa therapy have emerged as a major limitation of this otherwise effective therapy. Advancing medical and surgical treatment of these complications has been the main objective of clinical trials during the past few decades. In addition, basic research has focused on better understanding of the mechanisms of motor complications and how to prevent them. Slowing or delaying the progression of the disease delays the need for levodopa therapy; therefore, neuroprotective strategies may play an important role in preventing the onset and reducing the severity of levodopa-related adverse effects. In this introductory review, we present the rationale for current and experimental therapies designed to favorably modify the progression of PD. If implemented early in the course of the disease, such treatments, if found effective, may not only alter the natural progression of the disease but may also delay or minimize motor and nonmotor complications associated with levodopa.
DOI: 10.1002/mds.20457
PubMed: 15822111
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Levy Place, New York, NY 10029</wicri:regionArea></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="doi">10.1002/mds.20457</idno><idno type="RBID">pubmed:15822111</idno><idno type="pmid">15822111</idno><idno type="wicri:Area/PubMed/Corpus">003077</idno><idno type="wicri:Area/PubMed/Curation">003077</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neuroprotective therapy in Parkinson's disease and motor complications: a search for a pathogenesis-targeted, disease-modifying strategy.</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="1"><nlm:affiliation>Department of Neurology, Mount Sinai School of Medicine, Annenberg 14-94, One Gustave L. 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Levy Place, New York, NY 10029</wicri:regionArea></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal (therapeutic use)</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Coenzymes</term><term>Cyclooxygenase 1</term><term>Cyclooxygenase 2</term><term>Cyclooxygenase 2 Inhibitors</term><term>Cyclooxygenase Inhibitors (therapeutic use)</term><term>Dose-Response Relationship, Drug</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Dyskinesia, Drug-Induced (prevention & control)</term><term>Humans</term><term>Indans (therapeutic use)</term><term>Levodopa (adverse effects)</term><term>Levodopa (therapeutic use)</term><term>Membrane Proteins</term><term>N-Methylaspartate (antagonists & inhibitors)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Parkinson Disease (drug therapy)</term><term>Prostaglandin-Endoperoxide Synthases (metabolism)</term><term>Ubiquinone (analogs & derivatives)</term><term>Ubiquinone (therapeutic use)</term><term>Vitamin E (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Ubiquinone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>N-Methylaspartate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Prostaglandin-Endoperoxide Synthases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Antiparkinson Agents</term><term>Cyclooxygenase Inhibitors</term><term>Indans</term><term>Levodopa</term><term>Neuroprotective Agents</term><term>Ubiquinone</term><term>Vitamin E</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Coenzymes</term><term>Cyclooxygenase 1</term><term>Cyclooxygenase 2</term><term>Cyclooxygenase 2 Inhibitors</term><term>Membrane Proteins</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Dose-Response Relationship, Drug</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The introduction of levodopa in the late 1960s represented a landmark in the therapy of Parkinson's disease (PD). However, motor complications of chronic levodopa therapy have emerged as a major limitation of this otherwise effective therapy. Advancing medical and surgical treatment of these complications has been the main objective of clinical trials during the past few decades. In addition, basic research has focused on better understanding of the mechanisms of motor complications and how to prevent them. Slowing or delaying the progression of the disease delays the need for levodopa therapy; therefore, neuroprotective strategies may play an important role in preventing the onset and reducing the severity of levodopa-related adverse effects. In this introductory review, we present the rationale for current and experimental therapies designed to favorably modify the progression of PD. If implemented early in the course of the disease, such treatments, if found effective, may not only alter the natural progression of the disease but may also delay or minimize motor and nonmotor complications associated with levodopa.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">15822111</PMID><DateCreated><Year>2005</Year><Month>04</Month><Day>18</Day></DateCreated><DateCompleted><Year>2005</Year><Month>08</Month><Day>25</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>20 Suppl 11</Volume><PubDate><Year>2005</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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Slowing or delaying the progression of the disease delays the need for levodopa therapy; therefore, neuroprotective strategies may play an important role in preventing the onset and reducing the severity of levodopa-related adverse effects. In this introductory review, we present the rationale for current and experimental therapies designed to favorably modify the progression of PD. If implemented early in the course of the disease, such treatments, if found effective, may not only alter the natural progression of the disease but may also delay or minimize motor and nonmotor complications associated with levodopa.</AbstractText><CopyrightInformation>(c) 2005 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Olanow</LastName><ForeName>C Warren</ForeName><Initials>CW</Initials><AffiliationInfo><Affiliation>Department of Neurology, Mount Sinai School of Medicine, Annenberg 14-94, One Gustave L. 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