Milestones in Parkinson's Disease Therapeutics
Identifieur interne : 001A28 ( Main/Merge ); précédent : 001A27; suivant : 001A29Milestones 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.
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- Pascal (Inist)
English descriptors
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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 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.
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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><affiliations><list><country><li>Autriche</li><li>Canada</li><li>France</li><li>États-Unis</li></country><region><li>Midi-Pyrénées</li><li>Occitanie (région administrative)</li><li>Ontario</li><li>Pennsylvanie</li><li>Tyrol (Land)</li></region><settlement><li>Innsbruck</li><li>Toronto</li><li>Toulouse</li></settlement><orgName><li>Université de Toronto</li><li>Université de médecine d'Innsbruck</li></orgName></list><tree><country name="France"><region name="Occitanie (région administrative)"><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name></region></country><country name="Canada"><region name="Ontario"><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name></region></country><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name></region></country><country name="Autriche"><region name="Tyrol (Land)"><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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