ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000316

Milestones in Parkinson's Disease Therapeutics

Identifieur interne : 000316 ( PascalFrancis/Corpus ); précédent : 000315; suivant : 000317

Milestones in Parkinson's Disease Therapeutics

Auteurs : Olivier Rascol ; Andres Lozano ; Matthew Stern ; Werner Poewe

Source :

Movement disorders [ 0885-3185 ] ; 2011.

RBID : Pascal:11-0264661

Descripteurs français

Pascal (Inist)
- Maladie de Parkinson, Pathologie du système nerveux, Traitement, Lévodopa, Stimulant dopaminergique, Amine oxidase (flavin-containing), Stimulation cérébrale profonde.

English descriptors

KwdEn :
- Amine oxidase (flavin-containing), Deep brain stimulation, Dopamine agonist, Levodopa, Nervous system diseases, Parkinson disease, Treatment.

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A08	`01`	`1`	`ENG`	`@1 Milestones in Parkinson's Disease Therapeutics`
A11	`01`	`1`		`@1 RASCOL (Olivier)`
A11	`02`	`1`		`@1 LOZANO (Andres)`
A11	`03`	`1`		`@1 STERN (Matthew)`
A11	`04`	`1`		`@1 POEWE (Werner)`
A14	`01`			`@1 Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III @2 Toulouse @3 FRA @Z 1 aut.`
A14	`02`			`@1 Department of Neurosurgery, University of Toronto @2 Toronto, Ontario @3 CAN @Z 2 aut.`
A14	`03`			`@1 Department of Neurology, University of Pennsylvania @2 Philadelphia, Pennsylvania @3 USA @Z 3 aut.`
A14	`04`			`@1 Department of Neurology, Medical University of Innsbruck @2 Innsbruck @3 AUT @Z 4 aut.`
A20				`@1 1072-1082`
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A44				`@0 0000 @1 © 2011 INIST-CNRS. All rights reserved.`
A45				`@0 130 ref.`
A47	`01`	`1`		`@0 11-0264661`
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A61				`@0 A`
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C01	`01`		`ENG`	@0 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.
C02	`01`	`X`		`@0 002B17`
C02	`02`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Maladie de Parkinson @2 NM @5 01`
C03	`01`	`X`	`ENG`	`@0 Parkinson disease @2 NM @5 01`
C03	`01`	`X`	`SPA`	`@0 Parkinson enfermedad @2 NM @5 01`
C03	`02`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 02`
C03	`02`	`X`	`ENG`	`@0 Nervous system diseases @5 02`
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C03	`03`	`X`	`ENG`	`@0 Treatment @5 09`
C03	`03`	`X`	`SPA`	`@0 Tratamiento @5 09`
C03	`04`	`X`	`FRE`	`@0 Lévodopa @2 NK @2 FR @5 10`
C03	`04`	`X`	`ENG`	`@0 Levodopa @2 NK @2 FR @5 10`
C03	`04`	`X`	`SPA`	`@0 Levodopa @2 NK @2 FR @5 10`
C03	`05`	`X`	`FRE`	`@0 Stimulant dopaminergique @5 11`
C03	`05`	`X`	`ENG`	`@0 Dopamine agonist @5 11`
C03	`05`	`X`	`SPA`	`@0 Estimulante dopaminérgico @5 11`
C03	`06`	`X`	`FRE`	`@0 Amine oxidase (flavin-containing) @2 FE @5 12`
C03	`06`	`X`	`ENG`	`@0 Amine oxidase (flavin-containing) @2 FE @5 12`
C03	`06`	`X`	`SPA`	`@0 Amine oxidase (flavin-containing) @2 FE @5 12`
C03	`07`	`X`	`FRE`	`@0 Stimulation cérébrale profonde @4 CD @5 96`
C03	`07`	`X`	`ENG`	`@0 Deep brain stimulation @4 CD @5 96`
C07	`01`	`X`	`FRE`	`@0 Oxidoreductases @2 FE`
C07	`01`	`X`	`ENG`	`@0 Oxidoreductases @2 FE`
C07	`01`	`X`	`SPA`	`@0 Oxidoreductases @2 FE`
C07	`02`	`X`	`FRE`	`@0 Enzyme @2 FE`
C07	`02`	`X`	`ENG`	`@0 Enzyme @2 FE`
C07	`02`	`X`	`SPA`	`@0 Enzima @2 FE`
C07	`03`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 37`
C07	`03`	`X`	`ENG`	`@0 Cerebral disorder @5 37`
C07	`03`	`X`	`SPA`	`@0 Encéfalo patología @5 37`
C07	`04`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 38`
C07	`04`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 38`
C07	`04`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 38`
C07	`05`	`X`	`FRE`	`@0 Maladie dégénérative @5 39`
C07	`05`	`X`	`ENG`	`@0 Degenerative disease @5 39`
C07	`05`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 39`
C07	`06`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 40`
C07	`06`	`X`	`ENG`	`@0 Central nervous system disease @5 40`
C07	`06`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 40`
N21				`@1 178`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 11-0264661 INIST
ET :	Milestones in Parkinson's Disease Therapeutics
AU :	RASCOL (Olivier); LOZANO (Andres); STERN (Matthew); POEWE (Werner)
AF :	Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III/Toulouse/France (1 aut.); Department of Neurosurgery, University of Toronto/Toronto, Ontario/Canada (2 aut.); Department of Neurology, University of Pennsylvania/Philadelphia, Pennsylvania/Etats-Unis (3 aut.); Department of Neurology, Medical University of Innsbruck/Innsbruck/Autriche (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2011; Vol. 26; No. 6; Pp. 1072-1082; Bibl. 130 ref.
LA :	Anglais
EA :	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.
CC :	002B17; 002B17G
FD :	Maladie de Parkinson; Pathologie du système nerveux; Traitement; Lévodopa; Stimulant dopaminergique; Amine oxidase (flavin-containing); Stimulation cérébrale profonde
FG :	Oxidoreductases; Enzyme; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central
ED :	Parkinson disease; Nervous system diseases; Treatment; Levodopa; Dopamine agonist; Amine oxidase (flavin-containing); Deep brain stimulation
EG :	Oxidoreductases; Enzyme; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease
SD :	Parkinson enfermedad; Sistema nervioso patología; Tratamiento; Levodopa; Estimulante dopaminérgico; Amine oxidase (flavin-containing)
LO :	INIST-20953.354000191622890140
ID :	11-0264661

Links to Exploration step

Pascal:11-0264661

Le document en format XML

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<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>
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<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Dopamine agonist</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Estimulante dopaminérgico</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Amine oxidase (flavin-containing)</s0>
<s2>FE</s2>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Amine oxidase (flavin-containing)</s0>
<s2>FE</s2>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Amine oxidase (flavin-containing)</s0>
<s2>FE</s2>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Stimulation cérébrale profonde</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Deep brain stimulation</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fN21><s1>178</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 11-0264661 INIST</NO>
<ET>Milestones in Parkinson's Disease Therapeutics</ET>
<AU>RASCOL (Olivier); LOZANO (Andres); STERN (Matthew); POEWE (Werner)</AU>
<AF>Departments of Clinical Pharmacology and Neurosciences, University Hospital of Toulouse and Clinical Investigation Center INSERM CIC9302 and UMR825, University of Toulouse III/Toulouse/France (1 aut.); Department of Neurosurgery, University of Toronto/Toronto, Ontario/Canada (2 aut.); Department of Neurology, University of Pennsylvania/Philadelphia, Pennsylvania/Etats-Unis (3 aut.); Department of Neurology, Medical University of Innsbruck/Innsbruck/Autriche (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2011; Vol. 26; No. 6; Pp. 1072-1082; Bibl. 130 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17; 002B17G</CC>
<FD>Maladie de Parkinson; Pathologie du   système nerveux; Traitement; Lévodopa; Stimulant dopaminergique; Amine oxidase (flavin-containing); Stimulation cérébrale profonde</FD>
<FG>Oxidoreductases; Enzyme; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central</FG>
<ED>Parkinson disease; Nervous system diseases; Treatment; Levodopa; Dopamine agonist; Amine oxidase (flavin-containing); Deep brain stimulation</ED>
<EG>Oxidoreductases; Enzyme; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Parkinson enfermedad; Sistema nervioso patología; Tratamiento; Levodopa; Estimulante dopaminérgico; Amine oxidase (flavin-containing)</SD>
<LO>INIST-20953.354000191622890140</LO>
<ID>11-0264661</ID>
</server>
</inist>
</record>

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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Milestones in Parkinson's Disease Therapeutics

Milestones in Parkinson's Disease Therapeutics

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