ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000681

Dopamine Transporter Relation to Dopamine Turnover in Parkinson's Disease : A Positron Emission Tomography Study

Identifieur interne : 000681 ( PascalFrancis/Corpus ); précédent : 000680; suivant : 000682

Dopamine Transporter Relation to Dopamine Turnover in Parkinson's Disease : A Positron Emission Tomography Study

Auteurs : Vesna Sossi ; Raul De La Fuente-Fernandez ; Michael Schulzer ; Andre R. Troiano ; Thomas J. Ruth ; A. Jon Stoessl

Source :

Annals of neurology [ 0364-5134 ] ; 2007.

RBID : Pascal:08-0035341

Descripteurs français

Pascal (Inist)
- Pathologie du système nerveux, Maladie de Parkinson, Dopamine, Turnover, Tomoscintigraphie, Tomographie par émission de positons.

English descriptors

KwdEn :
- Dopamine, Emission tomography, Nervous system diseases, Parkinson disease, Positron emission tomography, Turnover.

Abstract

Objective: To investigate the role of the dopamine transporter (DAT) in the regulation of synaptic dopamine (DA) levels in Parkinson's disease and its role in the preservation of DA in presynaptic terminals. Methods: Ten Parkinson's disease patients (age, 62.9 ± 9.5 years; Unified Parkinson's Disease Rating Scale motor score in "off" state, 28.5 ± 8.2) underwent positron emission tomography with ¹¹C-methylphenidate (MP, a DAT marker), ¹¹C-dihydrotetrabenazine (a vesicular monoamine transporter 2 marker), and ¹⁸F-fluorodopa, leading to the determination of the MP and ¹¹C-dihydrotetrabenazine binding potentials (BPs) and the effective distribution volume for ¹⁸F-fluorodopa, the inverse of DA turnover. Seven patients also underwent positron emission tomography with ¹¹C-raclopride before and 1 hour after levodopa administration to estimate levodopa-induced changes in synaptic DA concentration. Results: We found a significant positive correlation between effective distribution volume and BP_MP (r = 0.93; p < 0.001) and a significant negative correlation between changes in synaptic DA concentration and BP_MP (r = -0.93; p = 0.04), independent of disease severity and duration. Interpretation: These data show that in Parkinson's disease, greater DAT levels are directly associated with lower DA turnover and lower changes in synaptic DA concentration. This implies that an important functional role of DAT is to maintain relatively constant synaptic DA levels and to preserve DA in nerve terminals. A decrease in DAT, although potentially serving as a compensatory mechanism in early disease, may ultimately result in increased DA turnover and higher oscillations in synaptic DA concentration, thereby possibly predisposing toward the occurrence of motor complications as disease progresses.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02	`01`			`@0 ANNED3`
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A05				`@2 62`
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A44				`@0 0000 @1 © 2008 INIST-CNRS. All rights reserved.`
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A61				`@0 A`
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C01	`01`		`ENG`	@0 Objective: To investigate the role of the dopamine transporter (DAT) in the regulation of synaptic dopamine (DA) levels in Parkinson's disease and its role in the preservation of DA in presynaptic terminals. Methods: Ten Parkinson's disease patients (age, 62.9 ± 9.5 years; Unified Parkinson's Disease Rating Scale motor score in "off" state, 28.5 ± 8.2) underwent positron emission tomography with ¹¹C-methylphenidate (MP, a DAT marker), ¹¹C-dihydrotetrabenazine (a vesicular monoamine transporter 2 marker), and ¹⁸F-fluorodopa, leading to the determination of the MP and ¹¹C-dihydrotetrabenazine binding potentials (BPs) and the effective distribution volume for ¹⁸F-fluorodopa, the inverse of DA turnover. Seven patients also underwent positron emission tomography with ¹¹C-raclopride before and 1 hour after levodopa administration to estimate levodopa-induced changes in synaptic DA concentration. Results: We found a significant positive correlation between effective distribution volume and BP_MP (r = 0.93; p < 0.001) and a significant negative correlation between changes in synaptic DA concentration and BP_MP (r = -0.93; p = 0.04), independent of disease severity and duration. Interpretation: These data show that in Parkinson's disease, greater DAT levels are directly associated with lower DA turnover and lower changes in synaptic DA concentration. This implies that an important functional role of DAT is to maintain relatively constant synaptic DA levels and to preserve DA in nerve terminals. A decrease in DAT, although potentially serving as a compensatory mechanism in early disease, may ultimately result in increased DA turnover and higher oscillations in synaptic DA concentration, thereby possibly predisposing toward the occurrence of motor complications as disease progresses.
C02	`01`	`X`		`@0 002B17`
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C03	`06`	`X`	`SPA`	`@0 Tomografía emisión positrones @5 12`
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C07	`02`	`X`	`FRE`	`@0 Neurotransmetteur @5 38`
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Format Inist (serveur)

NO :	PASCAL 08-0035341 INIST
ET :	Dopamine Transporter Relation to Dopamine Turnover in Parkinson's Disease : A Positron Emission Tomography Study
AU :	SOSSI (Vesna); DE LA FUENTE-FERNANDEZ (Raul); SCHULZER (Michael); TROIANO (Andre R.); RUTH (Thomas J.); STOESSL (A. Jon)
AF :	University of British Columbia/Vancouver, British Columbia/Canada (1 aut., 3 aut., 6 aut.); Division of Neurology, Hospital Arquitecto Marcide/Ferrol (A Coruña)/Espagne (2 aut.); Pacific Parkinson's Research Centre/Canada (4 aut., 6 aut.); TRIUMF/Vancouver, British Columbia/Canada (5 aut.)
DT :	Publication en série; Niveau analytique
SO :	Annals of neurology; ISSN 0364-5134; Coden ANNED3; Royaume-Uni; Da. 2007; Vol. 62; No. 5; Pp. 468-474; Bibl. 33 ref.
LA :	Anglais
EA :	Objective: To investigate the role of the dopamine transporter (DAT) in the regulation of synaptic dopamine (DA) levels in Parkinson's disease and its role in the preservation of DA in presynaptic terminals. Methods: Ten Parkinson's disease patients (age, 62.9 ± 9.5 years; Unified Parkinson's Disease Rating Scale motor score in "off" state, 28.5 ± 8.2) underwent positron emission tomography with ¹¹C-methylphenidate (MP, a DAT marker), ¹¹C-dihydrotetrabenazine (a vesicular monoamine transporter 2 marker), and ¹⁸F-fluorodopa, leading to the determination of the MP and ¹¹C-dihydrotetrabenazine binding potentials (BPs) and the effective distribution volume for ¹⁸F-fluorodopa, the inverse of DA turnover. Seven patients also underwent positron emission tomography with ¹¹C-raclopride before and 1 hour after levodopa administration to estimate levodopa-induced changes in synaptic DA concentration. Results: We found a significant positive correlation between effective distribution volume and BP_MP (r = 0.93; p < 0.001) and a significant negative correlation between changes in synaptic DA concentration and BP_MP (r = -0.93; p = 0.04), independent of disease severity and duration. Interpretation: These data show that in Parkinson's disease, greater DAT levels are directly associated with lower DA turnover and lower changes in synaptic DA concentration. This implies that an important functional role of DAT is to maintain relatively constant synaptic DA levels and to preserve DA in nerve terminals. A decrease in DAT, although potentially serving as a compensatory mechanism in early disease, may ultimately result in increased DA turnover and higher oscillations in synaptic DA concentration, thereby possibly predisposing toward the occurrence of motor complications as disease progresses.
CC :	002B17; 002B17G; 002B24B07
FD :	Pathologie du système nerveux; Maladie de Parkinson; Dopamine; Turnover; Tomoscintigraphie; Tomographie par émission de positons
FG :	Catécholamine; Neurotransmetteur; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central
ED :	Nervous system diseases; Parkinson disease; Dopamine; Turnover; Emission tomography; Positron emission tomography
EG :	Catecholamine; Neurotransmitter; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease
SD :	Sistema nervioso patología; Parkinson enfermedad; Dopamina; Turnover; Tomocentelleografía; Tomografía emisión positrones
LO :	INIST-16555.354000174350000070
ID :	08-0035341

Links to Exploration step

Pascal:08-0035341

Le document en format XML

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<front><div type="abstract" xml:lang="en">Objective: To investigate the role of the dopamine transporter (DAT) in the regulation of synaptic dopamine (DA) levels in Parkinson's disease and its role in the preservation of DA in presynaptic terminals. Methods: Ten Parkinson's disease patients (age, 62.9 ± 9.5 years; Unified Parkinson's Disease Rating Scale motor score in "off" state, 28.5 ± 8.2) underwent positron emission tomography with <sup>11</sup>
C-methylphenidate (MP, a DAT marker), <sup>11</sup>
C-dihydrotetrabenazine (a vesicular monoamine transporter 2 marker), and <sup>18</sup>
F-fluorodopa, leading to the determination of the MP and <sup>11</sup>
C-dihydrotetrabenazine binding potentials (BPs) and the effective distribution volume for <sup>18</sup>
F-fluorodopa, the inverse of DA turnover. Seven patients also underwent positron emission tomography with <sup>11</sup>
C-raclopride before and 1 hour after levodopa administration to estimate levodopa-induced changes in synaptic DA concentration. Results: We found a significant positive correlation between effective distribution volume and BP<sub>MP</sub>
 (r = 0.93; p < 0.001) and a significant negative correlation between changes in synaptic DA concentration and BP<sub>MP</sub>
 (r = -0.93; p = 0.04), independent of disease severity and duration. Interpretation: These data show that in Parkinson's disease, greater DAT levels are directly associated with lower DA turnover and lower changes in synaptic DA concentration. This implies that an important functional role of DAT is to maintain relatively constant synaptic DA levels and to preserve DA in nerve terminals. A decrease in DAT, although potentially serving as a compensatory mechanism in early disease, may ultimately result in increased DA turnover and higher oscillations in synaptic DA concentration, thereby possibly predisposing toward the occurrence of motor complications as disease progresses.</div>
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<fC01 i1="01" l="ENG"><s0>Objective: To investigate the role of the dopamine transporter (DAT) in the regulation of synaptic dopamine (DA) levels in Parkinson's disease and its role in the preservation of DA in presynaptic terminals. Methods: Ten Parkinson's disease patients (age, 62.9 ± 9.5 years; Unified Parkinson's Disease Rating Scale motor score in "off" state, 28.5 ± 8.2) underwent positron emission tomography with <sup>11</sup>
C-methylphenidate (MP, a DAT marker), <sup>11</sup>
C-dihydrotetrabenazine (a vesicular monoamine transporter 2 marker), and <sup>18</sup>
F-fluorodopa, leading to the determination of the MP and <sup>11</sup>
C-dihydrotetrabenazine binding potentials (BPs) and the effective distribution volume for <sup>18</sup>
F-fluorodopa, the inverse of DA turnover. Seven patients also underwent positron emission tomography with <sup>11</sup>
C-raclopride before and 1 hour after levodopa administration to estimate levodopa-induced changes in synaptic DA concentration. Results: We found a significant positive correlation between effective distribution volume and BP<sub>MP</sub>
 (r = 0.93; p < 0.001) and a significant negative correlation between changes in synaptic DA concentration and BP<sub>MP</sub>
 (r = -0.93; p = 0.04), independent of disease severity and duration. Interpretation: These data show that in Parkinson's disease, greater DAT levels are directly associated with lower DA turnover and lower changes in synaptic DA concentration. This implies that an important functional role of DAT is to maintain relatively constant synaptic DA levels and to preserve DA in nerve terminals. A decrease in DAT, although potentially serving as a compensatory mechanism in early disease, may ultimately result in increased DA turnover and higher oscillations in synaptic DA concentration, thereby possibly predisposing toward the occurrence of motor complications as disease progresses.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B24B07</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Pathologie du   système nerveux</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Turnover</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Turnover</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Turnover</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Tomoscintigraphie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Tomographie par émission de positons</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Positron emission tomography</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Tomografía emisión positrones</s0>
<s5>12</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fN21><s1>052</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
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<server><NO>PASCAL 08-0035341 INIST</NO>
<ET>Dopamine Transporter Relation to Dopamine Turnover in Parkinson's Disease : A Positron Emission Tomography Study</ET>
<AU>SOSSI (Vesna); DE LA FUENTE-FERNANDEZ (Raul); SCHULZER (Michael); TROIANO (Andre R.); RUTH (Thomas J.); STOESSL (A. Jon)</AU>
<AF>University of British Columbia/Vancouver, British Columbia/Canada (1 aut., 3 aut., 6 aut.); Division of Neurology, Hospital Arquitecto Marcide/Ferrol (A Coruña)/Espagne (2 aut.); Pacific Parkinson's Research Centre/Canada (4 aut., 6 aut.); TRIUMF/Vancouver, British Columbia/Canada (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Annals of neurology; ISSN 0364-5134; Coden ANNED3; Royaume-Uni; Da. 2007; Vol. 62; No. 5; Pp. 468-474; Bibl. 33 ref.</SO>
<LA>Anglais</LA>
<EA>Objective: To investigate the role of the dopamine transporter (DAT) in the regulation of synaptic dopamine (DA) levels in Parkinson's disease and its role in the preservation of DA in presynaptic terminals. Methods: Ten Parkinson's disease patients (age, 62.9 ± 9.5 years; Unified Parkinson's Disease Rating Scale motor score in "off" state, 28.5 ± 8.2) underwent positron emission tomography with <sup>11</sup>
C-methylphenidate (MP, a DAT marker), <sup>11</sup>
C-dihydrotetrabenazine (a vesicular monoamine transporter 2 marker), and <sup>18</sup>
F-fluorodopa, leading to the determination of the MP and <sup>11</sup>
C-dihydrotetrabenazine binding potentials (BPs) and the effective distribution volume for <sup>18</sup>
F-fluorodopa, the inverse of DA turnover. Seven patients also underwent positron emission tomography with <sup>11</sup>
C-raclopride before and 1 hour after levodopa administration to estimate levodopa-induced changes in synaptic DA concentration. Results: We found a significant positive correlation between effective distribution volume and BP<sub>MP</sub>
 (r = 0.93; p < 0.001) and a significant negative correlation between changes in synaptic DA concentration and BP<sub>MP</sub>
 (r = -0.93; p = 0.04), independent of disease severity and duration. Interpretation: These data show that in Parkinson's disease, greater DAT levels are directly associated with lower DA turnover and lower changes in synaptic DA concentration. This implies that an important functional role of DAT is to maintain relatively constant synaptic DA levels and to preserve DA in nerve terminals. A decrease in DAT, although potentially serving as a compensatory mechanism in early disease, may ultimately result in increased DA turnover and higher oscillations in synaptic DA concentration, thereby possibly predisposing toward the occurrence of motor complications as disease progresses.</EA>
<CC>002B17; 002B17G; 002B24B07</CC>
<FD>Pathologie du   système nerveux; Maladie de Parkinson; Dopamine; Turnover; Tomoscintigraphie; Tomographie par émission de positons</FD>
<FG>Catécholamine; Neurotransmetteur; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central</FG>
<ED>Nervous system diseases; Parkinson disease; Dopamine; Turnover; Emission tomography; Positron emission tomography</ED>
<EG>Catecholamine; Neurotransmitter; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Sistema nervioso patología; Parkinson enfermedad; Dopamina; Turnover; Tomocentelleografía; Tomografía emisión positrones</SD>
<LO>INIST-16555.354000174350000070</LO>
<ID>08-0035341</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)

Dopamine Transporter Relation to Dopamine Turnover in Parkinson's Disease : A Positron Emission Tomography Study

Dopamine Transporter Relation to Dopamine Turnover in Parkinson's Disease : A Positron Emission Tomography Study

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