Milestones in Parkinson's disease therapeutics
Identifieur interne : 001562 ( Main/Curation ); précédent : 001561; suivant : 001563Milestones in Parkinson's disease therapeutics
Auteurs : Olivier Rascol [France] ; Andres Lozano [Canada] ; Matthew Stern [États-Unis] ; Werner Poewe [Autriche]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-05.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Amantadine (history), Amantadine (therapeutic use), Amine oxidase (flavin-containing), Antiparkinson Agents (history), Antiparkinson Agents (therapeutic use), Deep Brain Stimulation (history), Deep Brain Stimulation (methods), Deep brain stimulation, Dopamine Agents (history), Dopamine Agents (therapeutic use), Dopamine agonist, Enzyme Inhibitors (history), Enzyme Inhibitors (therapeutic use), History, 19th Century, History, 20th Century, History, 21st Century, Humans, Levodopa, Nervous system diseases, Pallidotomy (history), Pallidotomy (methods), Parkinson Disease (complications), Parkinson Disease (history), Parkinson Disease (therapy), Parkinson disease, Parkinson's disease, Treatment, catecholmethyltransferase inhibitors, deep brain stimulation, dopamine agonists, levodopa, monoamine oxidase B inhibitors, treatment.
- MESH :
- chemical , history : Amantadine, Antiparkinson Agents, Dopamine Agents, Enzyme Inhibitors.
- chemical , therapeutic use : Amantadine, Antiparkinson Agents, Dopamine Agents, Enzyme Inhibitors.
- complications : Parkinson Disease.
- history : Deep Brain Stimulation, Pallidotomy, Parkinson Disease.
- methods : Deep Brain Stimulation, Pallidotomy.
- therapy : Parkinson Disease.
- History, 19th Century, History, 20th Century, History, 21st Century, Humans.
Abstract
In the mid‐1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23714
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ISTEX:A1E9CDE32413AB1BF3B0752267721A147AA6986DLe document en format XML
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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="2011-05">2011-05</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1072">1072</biblScope><biblScope unit="page" to="1082">1082</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">A1E9CDE32413AB1BF3B0752267721A147AA6986D</idno><idno type="DOI">10.1002/mds.23714</idno><idno type="ArticleID">MDS23714</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amantadine (history)</term><term>Amantadine (therapeutic use)</term><term>Amine oxidase (flavin-containing)</term><term>Antiparkinson Agents (history)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Deep Brain Stimulation (history)</term><term>Deep Brain Stimulation (methods)</term><term>Deep brain stimulation</term><term>Dopamine Agents (history)</term><term>Dopamine Agents (therapeutic use)</term><term>Dopamine agonist</term><term>Enzyme Inhibitors (history)</term><term>Enzyme Inhibitors (therapeutic use)</term><term>History, 19th Century</term><term>History, 20th Century</term><term>History, 21st Century</term><term>Humans</term><term>Levodopa</term><term>Nervous system diseases</term><term>Pallidotomy (history)</term><term>Pallidotomy (methods)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (history)</term><term>Parkinson Disease (therapy)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Treatment</term><term>catecholmethyltransferase inhibitors</term><term>deep brain stimulation</term><term>dopamine agonists</term><term>levodopa</term><term>monoamine oxidase B inhibitors</term><term>treatment</term></keywords><keywords scheme="MESH" type="chemical" qualifier="history" xml:lang="en"><term>Amantadine</term><term>Antiparkinson Agents</term><term>Dopamine Agents</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Amantadine</term><term>Antiparkinson Agents</term><term>Dopamine Agents</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="history" xml:lang="en"><term>Deep Brain Stimulation</term><term>Pallidotomy</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term><term>Pallidotomy</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>History, 19th Century</term><term>History, 20th Century</term><term>History, 21st Century</term><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Amine oxidase (flavin-containing)</term><term>Lévodopa</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Stimulant dopaminergique</term><term>Stimulation cérébrale profonde</term><term>Traitement</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the mid‐1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society</div></front></TEI><double idat="0885-3185:2011:Rascol O:milestones:in:parkinson"><INIST><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Milestones in Parkinson's Disease Therapeutics</title><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III</s1><s2>Toulouse</s2><s3>FRA</s3><sZ>1 aut.</sZ></inist:fA14><country>France</country><placeName><settlement type="city">Toulouse</settlement></placeName><placeName><settlement type="city">Toulouse</settlement><region type="region" nuts="2">Midi-Pyrénées</region></placeName><orgName type="university" n="3">Université Toulouse III - Paul Sabatier</orgName><orgName type="institution" wicri:auto="newGroup">Université de Toulouse</orgName></affiliation></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Neurosurgery, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurology, University of Pennsylvania</s1><s2>Philadelphia, Pennsylvania</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation wicri:level="4"><inist:fA14 i1="04"><s1>Department of Neurology, Medical University of Innsbruck</s1><s2>Innsbruck</s2><s3>AUT</s3><sZ>4 aut.</sZ></inist:fA14><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">11-0264661</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 11-0264661 INIST</idno><idno type="RBID">Pascal:11-0264661</idno><idno type="wicri:Area/PascalFrancis/Corpus">000567</idno><idno type="wicri:Area/PascalFrancis/Curation">002751</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000512</idno><idno type="wicri:doubleKey">0885-3185:2011:Rascol O:milestones:in:parkinson</idno><idno type="wicri:Area/Main/Merge">001B02</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Milestones in Parkinson's Disease Therapeutics</title><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III</s1><s2>Toulouse</s2><s3>FRA</s3><sZ>1 aut.</sZ></inist:fA14><country>France</country><placeName><settlement type="city">Toulouse</settlement></placeName><placeName><settlement type="city">Toulouse</settlement><region type="region" nuts="2">Midi-Pyrénées</region></placeName><orgName type="university" n="3">Université Toulouse III - Paul Sabatier</orgName><orgName type="institution" wicri:auto="newGroup">Université de Toulouse</orgName></affiliation></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Neurosurgery, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurology, University of Pennsylvania</s1><s2>Philadelphia, Pennsylvania</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation wicri:level="4"><inist:fA14 i1="04"><s1>Department of Neurology, Medical University of Innsbruck</s1><s2>Innsbruck</s2><s3>AUT</s3><sZ>4 aut.</sZ></inist:fA14><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amine oxidase (flavin-containing)</term><term>Deep brain stimulation</term><term>Dopamine agonist</term><term>Levodopa</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Traitement</term><term>Lévodopa</term><term>Stimulant dopaminergique</term><term>Amine oxidase (flavin-containing)</term><term>Stimulation cérébrale profonde</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the mid-1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug-refractory levodopa-induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an anti-dyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions.</div></front></TEI></INIST><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Milestones in Parkinson's disease therapeutics</title><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name><affiliation><country>France</country><placeName><settlement type="city">Toulouse</settlement><region type="region" nuts="2">Midi-Pyrénées</region></placeName><orgName type="university" n="3">Université Toulouse III - Paul Sabatier</orgName><orgName type="institution" wicri:auto="newGroup">Université de Toulouse</orgName></affiliation></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name></author><author><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A1E9CDE32413AB1BF3B0752267721A147AA6986D</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23714</idno><idno type="url">https://api.istex.fr/document/A1E9CDE32413AB1BF3B0752267721A147AA6986D/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000157</idno><idno type="wicri:Area/Istex/Curation">000157</idno><idno type="wicri:Area/Istex/Checkpoint">000294</idno><idno type="wicri:doubleKey">0885-3185:2011:Rascol O:milestones:in:parkinson</idno><idno type="wicri:source">PubMed</idno><idno type="RBID">pubmed:21626552</idno><idno type="wicri:Area/PubMed/Corpus">001170</idno><idno type="wicri:Area/PubMed/Curation">001170</idno><idno type="wicri:Area/PubMed/Checkpoint">001246</idno><idno type="wicri:Area/Ncbi/Merge">003258</idno><idno type="wicri:Area/Ncbi/Curation">003258</idno><idno type="wicri:Area/Ncbi/Checkpoint">003258</idno><idno type="wicri:Area/Main/Merge">001615</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Milestones in Parkinson's disease therapeutics</title><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III, Toulouse</wicri:regionArea><placeName><settlement type="city">Toulouse</settlement></placeName><placeName><settlement type="city">Toulouse</settlement><region type="region" nuts="2">Midi-Pyrénées</region></placeName><orgName type="university" n="3">Université Toulouse III - Paul Sabatier</orgName><orgName type="institution" wicri:auto="newGroup">Université de Toulouse</orgName></affiliation></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Neurosurgery, University of Toronto, Toronto, Ontario</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation wicri:level="4"><country xml:lang="fr">Autriche</country><wicri:regionArea>Department of Neurology, Medical University of Innsbruck, Innsbruck</wicri:regionArea><orgName type="university">Université de médecine d'Innsbruck</orgName><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</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="2011-05">2011-05</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1072">1072</biblScope><biblScope unit="page" to="1082">1082</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">A1E9CDE32413AB1BF3B0752267721A147AA6986D</idno><idno type="DOI">10.1002/mds.23714</idno><idno type="ArticleID">MDS23714</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amantadine (history)</term><term>Amantadine (therapeutic use)</term><term>Antiparkinson Agents (history)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Deep Brain Stimulation (history)</term><term>Deep Brain Stimulation (methods)</term><term>Dopamine Agents (history)</term><term>Dopamine Agents (therapeutic use)</term><term>Enzyme Inhibitors (history)</term><term>Enzyme Inhibitors (therapeutic use)</term><term>History, 19th Century</term><term>History, 20th Century</term><term>History, 21st Century</term><term>Humans</term><term>Pallidotomy (history)</term><term>Pallidotomy (methods)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (history)</term><term>Parkinson Disease (therapy)</term><term>Parkinson's disease</term><term>catecholmethyltransferase inhibitors</term><term>deep brain stimulation</term><term>dopamine agonists</term><term>levodopa</term><term>monoamine oxidase B inhibitors</term><term>treatment</term></keywords><keywords scheme="MESH" type="chemical" qualifier="history" xml:lang="en"><term>Amantadine</term><term>Antiparkinson Agents</term><term>Dopamine Agents</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Amantadine</term><term>Antiparkinson Agents</term><term>Dopamine Agents</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="history" xml:lang="en"><term>Deep Brain Stimulation</term><term>Pallidotomy</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term><term>Pallidotomy</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>History, 19th Century</term><term>History, 20th Century</term><term>History, 21st Century</term><term>Humans</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the mid‐1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug‐refractory levodopa‐induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions. © 2011 Movement Disorder Society</div></front></TEI></ISTEX></double></record>Pour manipuler ce document sous Unix (Dilib)
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