ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000D07

In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease

Identifieur interne : 000D07 ( PascalFrancis/Corpus ); précédent : 000D06; suivant : 000D08

In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease

Auteurs : C. S. Lee ; A. Samii ; V. Sossi ; T. J. Ruth ; M. Schulzer ; J. E. Holden ; J. Wudel ; P. K. Pal ; R. De La Fuente-Fernandez ; D. B. Calne ; A. J. Stoessl

Source :

Annals of neurology [ 0364-5134 ] ; 2000.

RBID : Pascal:00-0211896

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Tomoscintigraphie, Positon, Terminaison nerveuse présynaptique, Neurone dopaminergique, Corps strié, In vivo, Exploration, Homme.

English descriptors

KwdEn :
- Corpus striatum, Dopaminergic neuron, Emission tomography, Exploration, Human, In vivo, Parkinson disease, Positron, Presynaptic nerve ending.

Abstract

Clinical symptoms of Parkinson's disease (PD) do not manifest until dopamine (DA) neuronal loss reaches a symptomatic threshold. To explore the mechanisms of functional compensation that occur in presynaptic DA nerve terminals in PD, we compared striatal positron emission tomographic (PET) measurements by using ["C]dihydrotetrabenazine ([¹¹C]DTBZ; labeling the vesicular monoamine transporter type 2), [¹¹C]methylphenidate (labeling the plasma membrane DA transporter), and [¹⁸F]dopa (reflecting synthesis and storage of DA). Three consecutive PET scans were performed in three-dimensional mode by using each tracer on 35 patients and 16 age-matched, normal controls. PET measurements by the three tracers were compared between subgroups of earlier and later stages of PD, between drug-naive and drug-treated subgroups of PD, and between subregions of the parkinsonian striatum. The quantitative relationships of [¹⁸F]dopa and [¹¹C]DTBZ, and of [¹¹C]methylphenidate and [¹¹C]DTBZ, were compared between the PD and the normal control subjects. We found that [¹⁸F]dopa K_i was reduced less than the binding potential (B_max/K_d) for ["C]DTBZ in the parkinsonian striatum, whereas the [¹¹C]methylphenidate binding potential was reduced more than [¹¹C]DTBZ binding potential. These observations suggest that the activity of aromatic L-amino acid decarboxylase is up-regulated, whereas the plasma membrane DA transporter is down-regulated in the striatum of patients with PD.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A14	`02`			`@1 TRIUMF, University of British Columbia @2 Vancouver, British Columbia @3 CAN @Z 3 aut. @Z 4 aut.`
A14	`03`			`@1 Department of Medical Physics, University of Wisconsin @2 Madison, WI @3 USA @Z 6 aut.`
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C01	`01`		`ENG`	@0 Clinical symptoms of Parkinson's disease (PD) do not manifest until dopamine (DA) neuronal loss reaches a symptomatic threshold. To explore the mechanisms of functional compensation that occur in presynaptic DA nerve terminals in PD, we compared striatal positron emission tomographic (PET) measurements by using ["C]dihydrotetrabenazine ([¹¹C]DTBZ; labeling the vesicular monoamine transporter type 2), [¹¹C]methylphenidate (labeling the plasma membrane DA transporter), and [¹⁸F]dopa (reflecting synthesis and storage of DA). Three consecutive PET scans were performed in three-dimensional mode by using each tracer on 35 patients and 16 age-matched, normal controls. PET measurements by the three tracers were compared between subgroups of earlier and later stages of PD, between drug-naive and drug-treated subgroups of PD, and between subregions of the parkinsonian striatum. The quantitative relationships of [¹⁸F]dopa and [¹¹C]DTBZ, and of [¹¹C]methylphenidate and [¹¹C]DTBZ, were compared between the PD and the normal control subjects. We found that [¹⁸F]dopa K_i was reduced less than the binding potential (B_max/K_d) for ["C]DTBZ in the parkinsonian striatum, whereas the [¹¹C]methylphenidate binding potential was reduced more than [¹¹C]DTBZ binding potential. These observations suggest that the activity of aromatic L-amino acid decarboxylase is up-regulated, whereas the plasma membrane DA transporter is down-regulated in the striatum of patients with PD.
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Format Inist (serveur)

NO :	PASCAL 00-0211896 INIST
ET :	In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease
AU :	LEE (C. S.); SAMII (A.); SOSSI (V.); RUTH (T. J.); SCHULZER (M.); HOLDEN (J. E.); WUDEL (J.); PAL (P. K.); DE LA FUENTE-FERNANDEZ (R.); CALNE (D. B.); STOESSL (A. J.)
AF :	Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre/Vancouver, British Columbia/Canada (1 aut., 2 aut., 5 aut., 7 aut., 8 aut., 9 aut., 10 aut., 11 aut.); TRIUMF, University of British Columbia/Vancouver, British Columbia/Canada (3 aut., 4 aut.); Department of Medical Physics, University of Wisconsin/Madison, WI/Etats-Unis (6 aut.)
DT :	Publication en série; Niveau analytique
SO :	Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2000; Vol. 47; No. 4; Pp. 493-503; Bibl. 84 ref.
LA :	Anglais
EA :	Clinical symptoms of Parkinson's disease (PD) do not manifest until dopamine (DA) neuronal loss reaches a symptomatic threshold. To explore the mechanisms of functional compensation that occur in presynaptic DA nerve terminals in PD, we compared striatal positron emission tomographic (PET) measurements by using ["C]dihydrotetrabenazine ([¹¹C]DTBZ; labeling the vesicular monoamine transporter type 2), [¹¹C]methylphenidate (labeling the plasma membrane DA transporter), and [¹⁸F]dopa (reflecting synthesis and storage of DA). Three consecutive PET scans were performed in three-dimensional mode by using each tracer on 35 patients and 16 age-matched, normal controls. PET measurements by the three tracers were compared between subgroups of earlier and later stages of PD, between drug-naive and drug-treated subgroups of PD, and between subregions of the parkinsonian striatum. The quantitative relationships of [¹⁸F]dopa and [¹¹C]DTBZ, and of [¹¹C]methylphenidate and [¹¹C]DTBZ, were compared between the PD and the normal control subjects. We found that [¹⁸F]dopa K_i was reduced less than the binding potential (B_max/K_d) for ["C]DTBZ in the parkinsonian striatum, whereas the [¹¹C]methylphenidate binding potential was reduced more than [¹¹C]DTBZ binding potential. These observations suggest that the activity of aromatic L-amino acid decarboxylase is up-regulated, whereas the plasma membrane DA transporter is down-regulated in the striatum of patients with PD.
CC :	002B17G
FD :	Parkinson maladie; Tomoscintigraphie; Positon; Terminaison nerveuse présynaptique; Neurone dopaminergique; Corps strié; In vivo; Exploration; Homme
FG :	Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique; Encéphale
ED :	Parkinson disease; Emission tomography; Positron; Presynaptic nerve ending; Dopaminergic neuron; Corpus striatum; In vivo; Exploration; Human
EG :	Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study; Brain (vertebrata)
SD :	Parkinson enfermedad; Tomocentelleografía; Positrón; Terminación nerviosa presináptica; Neurona dopaminérgica; Cuerpo estriado; In vivo; Exploración; Hombre
LO :	INIST-16555.354000082307330130
ID :	00-0211896

Links to Exploration step

Pascal:00-0211896

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease</title>
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<author><name sortKey="Pal, P K" sort="Pal, P K" uniqKey="Pal P" first="P. K." last="Pal">P. K. Pal</name>
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<author><name sortKey="De La Fuente Fernandez, R" sort="De La Fuente Fernandez, R" uniqKey="De La Fuente Fernandez R" first="R." last="De La Fuente-Fernandez">R. De La Fuente-Fernandez</name>
<affiliation><inist:fA14 i1="01"><s1>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre</s1>
<s2>Vancouver, British Columbia</s2>
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<sZ>1 aut.</sZ>
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<author><name sortKey="Calne, D B" sort="Calne, D B" uniqKey="Calne D" first="D. B." last="Calne">D. B. Calne</name>
<affiliation><inist:fA14 i1="01"><s1>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre</s1>
<s2>Vancouver, British Columbia</s2>
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<sZ>1 aut.</sZ>
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<series><title level="j" type="main">Annals of neurology</title>
<title level="j" type="abbreviated">Ann. neurol.</title>
<idno type="ISSN">0364-5134</idno>
<imprint><date when="2000">2000</date>
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<seriesStmt><title level="j" type="main">Annals of neurology</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Corpus striatum</term>
<term>Dopaminergic neuron</term>
<term>Emission tomography</term>
<term>Exploration</term>
<term>Human</term>
<term>In vivo</term>
<term>Parkinson disease</term>
<term>Positron</term>
<term>Presynaptic nerve ending</term>
</keywords>
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<term>Tomoscintigraphie</term>
<term>Positon</term>
<term>Terminaison nerveuse présynaptique</term>
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<front><div type="abstract" xml:lang="en">Clinical symptoms of Parkinson's disease (PD) do not manifest until dopamine (DA) neuronal loss reaches a symptomatic threshold. To explore the mechanisms of functional compensation that occur in presynaptic DA nerve terminals in PD, we compared striatal positron emission tomographic (PET) measurements by using ["C]dihydrotetrabenazine ([<sup>11</sup>
C]DTBZ; labeling the vesicular monoamine transporter type 2), [<sup>11</sup>
C]methylphenidate (labeling the plasma membrane DA transporter), and [<sup>18</sup>
F]dopa (reflecting synthesis and storage of DA). Three consecutive PET scans were performed in three-dimensional mode by using each tracer on 35 patients and 16 age-matched, normal controls. PET measurements by the three tracers were compared between subgroups of earlier and later stages of PD, between drug-naive and drug-treated subgroups of PD, and between subregions of the parkinsonian striatum. The quantitative relationships of [<sup>18</sup>
F]dopa and [<sup>11</sup>
C]DTBZ, and of [<sup>11</sup>
C]methylphenidate and [<sup>11</sup>
C]DTBZ, were compared between the PD and the normal control subjects. We found that [<sup>18</sup>
F]dopa K<sub>i</sub>
 was reduced less than the binding potential (B<sub>max</sub>
/K<sub>d</sub>
) for ["C]DTBZ in the parkinsonian striatum, whereas the [<sup>11</sup>
C]methylphenidate binding potential was reduced more than [<sup>11</sup>
C]DTBZ binding potential. These observations suggest that the activity of aromatic L-amino acid decarboxylase is up-regulated, whereas the plasma membrane DA transporter is down-regulated in the striatum of patients with PD.</div>
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<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
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<fA14 i1="02"><s1>TRIUMF, University of British Columbia</s1>
<s2>Vancouver, British Columbia</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Medical Physics, University of Wisconsin</s1>
<s2>Madison, WI</s2>
<s3>USA</s3>
<sZ>6 aut.</sZ>
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C]DTBZ; labeling the vesicular monoamine transporter type 2), [<sup>11</sup>
C]methylphenidate (labeling the plasma membrane DA transporter), and [<sup>18</sup>
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F]dopa and [<sup>11</sup>
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/K<sub>d</sub>
) for ["C]DTBZ in the parkinsonian striatum, whereas the [<sup>11</sup>
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<ET>In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease</ET>
<AU>LEE (C. S.); SAMII (A.); SOSSI (V.); RUTH (T. J.); SCHULZER (M.); HOLDEN (J. E.); WUDEL (J.); PAL (P. K.); DE LA FUENTE-FERNANDEZ (R.); CALNE (D. B.); STOESSL (A. J.)</AU>
<AF>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre/Vancouver, British Columbia/Canada (1 aut., 2 aut., 5 aut., 7 aut., 8 aut., 9 aut., 10 aut., 11 aut.); TRIUMF, University of British Columbia/Vancouver, British Columbia/Canada (3 aut., 4 aut.); Department of Medical Physics, University of Wisconsin/Madison, WI/Etats-Unis (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2000; Vol. 47; No. 4; Pp. 493-503; Bibl. 84 ref.</SO>
<LA>Anglais</LA>
<EA>Clinical symptoms of Parkinson's disease (PD) do not manifest until dopamine (DA) neuronal loss reaches a symptomatic threshold. To explore the mechanisms of functional compensation that occur in presynaptic DA nerve terminals in PD, we compared striatal positron emission tomographic (PET) measurements by using ["C]dihydrotetrabenazine ([<sup>11</sup>
C]DTBZ; labeling the vesicular monoamine transporter type 2), [<sup>11</sup>
C]methylphenidate (labeling the plasma membrane DA transporter), and [<sup>18</sup>
F]dopa (reflecting synthesis and storage of DA). Three consecutive PET scans were performed in three-dimensional mode by using each tracer on 35 patients and 16 age-matched, normal controls. PET measurements by the three tracers were compared between subgroups of earlier and later stages of PD, between drug-naive and drug-treated subgroups of PD, and between subregions of the parkinsonian striatum. The quantitative relationships of [<sup>18</sup>
F]dopa and [<sup>11</sup>
C]DTBZ, and of [<sup>11</sup>
C]methylphenidate and [<sup>11</sup>
C]DTBZ, were compared between the PD and the normal control subjects. We found that [<sup>18</sup>
F]dopa K<sub>i</sub>
 was reduced less than the binding potential (B<sub>max</sub>
/K<sub>d</sub>
) for ["C]DTBZ in the parkinsonian striatum, whereas the [<sup>11</sup>
C]methylphenidate binding potential was reduced more than [<sup>11</sup>
C]DTBZ binding potential. These observations suggest that the activity of aromatic L-amino acid decarboxylase is up-regulated, whereas the plasma membrane DA transporter is down-regulated in the striatum of patients with PD.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Tomoscintigraphie; Positon; Terminaison nerveuse présynaptique; Neurone dopaminergique; Corps strié; In vivo; Exploration; Homme</FD>
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<ED>Parkinson disease; Emission tomography; Positron; Presynaptic nerve ending; Dopaminergic neuron; Corpus striatum; In vivo; Exploration; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study; Brain (vertebrata)</EG>
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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)

In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease

In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease

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