Parkinson's disease duration determines effect of dopaminergic therapy on ventral striatum function.
Identifieur interne : 000861 ( Main/Exploration ); précédent : 000860; suivant : 000862Parkinson's disease duration determines effect of dopaminergic therapy on ventral striatum function.
Auteurs : Alex A. Macdonald [Canada] ; Oury Monchi ; Ken N. Seergobin ; Hooman Ganjavi ; Ruzbeh Tamjeedi ; Penny A. MacdonaldSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Age Factors, Age of Onset, Aged, Analysis of Variance, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (adverse effects), Antiparkinson Agents (therapeutic use), Basal Ganglia (physiopathology), Computers, Dopamine (physiology), Dopamine Agents (administration & dosage), Dopamine Agents (adverse effects), Dopamine Agents (therapeutic use), Educational Status, Female, Humans, Learning, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Photic Stimulation, Psychomotor Performance (physiology), Reward.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Dopamine Agents.
- chemical , adverse effects : Antiparkinson Agents, Dopamine Agents.
- chemical , physiology : Dopamine.
- chemical , therapeutic use : Antiparkinson Agents, Dopamine Agents.
- drug therapy : Parkinson Disease.
- physiology : Psychomotor Performance.
- physiopathology : Basal Ganglia, Parkinson Disease.
- Age Factors, Age of Onset, Aged, Analysis of Variance, Computers, Educational Status, Female, Humans, Learning, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Photic Stimulation, Reward.
Abstract
We investigated the hypothesis that variation in endogenous dopamine (DA) across brain regions explains dissimilar effects of dopaminergic therapy on aspects of cognition in early Parkinson's disease (PD). Extensive degeneration of DA-producing cells in the substantia nigra cause dorsal striatum (DS) DA deficiency and movement abnormalities. Particularly in early PD, this contrasts with relative sparing of the dopaminergic cells of the ventral tegmental area (VTA). The hypothesis predicts that DS-mediated cognitive functions are deficient at baseline and improved by DA replacement, whereas functions depending upon VTA-innervated brain regions are normal off medication and worsen with treatment. The latter pattern presumably owes to overdose of relatively DA-replete VTA-supplied brain regions with medication levels titrated to DS-mediated motor symptoms. As PD progresses, however, VTA degeneration increases. Impairment in cognitive operations performed by VTA-innervated brain regions, such as the ventral striatum (VS), is expected. We compared the performance of early and late PD patients, on and off dopaminergic medication, relative to age-matched controls, on reward learning, previously shown to implicate the VS. As expected, in early PD, stimulus-reward learning was normal off medication, but worsened with DA replacement. At more advanced disease stages, PD patients learned stimulus-reward contingencies more poorly than controls and early PD patients off medication. Furthermore, dopaminergic medication did not worsen reward learning in late PD patients, in line with the dopamine overdose hypothesis. Unlike its effect on DS-mediated functions, however, DA-replacement therapy did not improve reward learning in late PD patients.
DOI: 10.1002/mds.25152
PubMed: 23165957
Affiliations:
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Macdonald</name><affiliation wicri:level="4"><nlm:affiliation>Department of Psychology, McGill University, Montreal, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Psychology, McGill University, Montreal, Quebec</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Monchi, Oury" sort="Monchi, Oury" uniqKey="Monchi O" first="Oury" last="Monchi">Oury Monchi</name></author><author><name sortKey="Seergobin, Ken N" sort="Seergobin, Ken N" uniqKey="Seergobin K" first="Ken N" last="Seergobin">Ken N. Seergobin</name></author><author><name sortKey="Ganjavi, Hooman" sort="Ganjavi, Hooman" uniqKey="Ganjavi H" first="Hooman" last="Ganjavi">Hooman Ganjavi</name></author><author><name sortKey="Tamjeedi, Ruzbeh" sort="Tamjeedi, Ruzbeh" uniqKey="Tamjeedi R" first="Ruzbeh" last="Tamjeedi">Ruzbeh Tamjeedi</name></author><author><name sortKey="Macdonald, Penny A" sort="Macdonald, Penny A" uniqKey="Macdonald P" first="Penny A" last="Macdonald">Penny A. 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Macdonald</name><affiliation wicri:level="4"><nlm:affiliation>Department of Psychology, McGill University, Montreal, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Psychology, McGill University, Montreal, Quebec</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Monchi, Oury" sort="Monchi, Oury" uniqKey="Monchi O" first="Oury" last="Monchi">Oury Monchi</name></author><author><name sortKey="Seergobin, Ken N" sort="Seergobin, Ken N" uniqKey="Seergobin K" first="Ken N" last="Seergobin">Ken N. Seergobin</name></author><author><name sortKey="Ganjavi, Hooman" sort="Ganjavi, Hooman" uniqKey="Ganjavi H" first="Hooman" last="Ganjavi">Hooman Ganjavi</name></author><author><name sortKey="Tamjeedi, Ruzbeh" sort="Tamjeedi, Ruzbeh" uniqKey="Tamjeedi R" first="Ruzbeh" last="Tamjeedi">Ruzbeh Tamjeedi</name></author><author><name sortKey="Macdonald, Penny A" sort="Macdonald, Penny A" uniqKey="Macdonald P" first="Penny A" last="Macdonald">Penny A. Macdonald</name></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="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors</term><term>Age of Onset</term><term>Aged</term><term>Analysis of Variance</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Basal Ganglia (physiopathology)</term><term>Computers</term><term>Dopamine (physiology)</term><term>Dopamine Agents (administration & dosage)</term><term>Dopamine Agents (adverse effects)</term><term>Dopamine Agents (therapeutic use)</term><term>Educational Status</term><term>Female</term><term>Humans</term><term>Learning</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Photic Stimulation</term><term>Psychomotor Performance (physiology)</term><term>Reward</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agents</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>Psychomotor Performance</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Age of Onset</term><term>Aged</term><term>Analysis of Variance</term><term>Computers</term><term>Educational Status</term><term>Female</term><term>Humans</term><term>Learning</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Photic Stimulation</term><term>Reward</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated the hypothesis that variation in endogenous dopamine (DA) across brain regions explains dissimilar effects of dopaminergic therapy on aspects of cognition in early Parkinson's disease (PD). Extensive degeneration of DA-producing cells in the substantia nigra cause dorsal striatum (DS) DA deficiency and movement abnormalities. Particularly in early PD, this contrasts with relative sparing of the dopaminergic cells of the ventral tegmental area (VTA). The hypothesis predicts that DS-mediated cognitive functions are deficient at baseline and improved by DA replacement, whereas functions depending upon VTA-innervated brain regions are normal off medication and worsen with treatment. The latter pattern presumably owes to overdose of relatively DA-replete VTA-supplied brain regions with medication levels titrated to DS-mediated motor symptoms. As PD progresses, however, VTA degeneration increases. Impairment in cognitive operations performed by VTA-innervated brain regions, such as the ventral striatum (VS), is expected. We compared the performance of early and late PD patients, on and off dopaminergic medication, relative to age-matched controls, on reward learning, previously shown to implicate the VS. As expected, in early PD, stimulus-reward learning was normal off medication, but worsened with DA replacement. At more advanced disease stages, PD patients learned stimulus-reward contingencies more poorly than controls and early PD patients off medication. Furthermore, dopaminergic medication did not worsen reward learning in late PD patients, in line with the dopamine overdose hypothesis. Unlike its effect on DS-mediated functions, however, DA-replacement therapy did not improve reward learning in late PD patients.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><noCountry><name sortKey="Ganjavi, Hooman" sort="Ganjavi, Hooman" uniqKey="Ganjavi H" first="Hooman" last="Ganjavi">Hooman Ganjavi</name><name sortKey="Macdonald, Penny A" sort="Macdonald, Penny A" uniqKey="Macdonald P" first="Penny A" last="Macdonald">Penny A. Macdonald</name><name sortKey="Monchi, Oury" sort="Monchi, Oury" uniqKey="Monchi O" first="Oury" last="Monchi">Oury Monchi</name><name sortKey="Seergobin, Ken N" sort="Seergobin, Ken N" uniqKey="Seergobin K" first="Ken N" last="Seergobin">Ken N. Seergobin</name><name sortKey="Tamjeedi, Ruzbeh" sort="Tamjeedi, Ruzbeh" uniqKey="Tamjeedi R" first="Ruzbeh" last="Tamjeedi">Ruzbeh Tamjeedi</name></noCountry><country name="Canada"><region name="Québec"><name sortKey="Macdonald, Alex A" sort="Macdonald, Alex A" uniqKey="Macdonald A" first="Alex A" last="Macdonald">Alex A. Macdonald</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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