In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease.
Identifieur interne : 001645 ( PubMed/Curation ); précédent : 001644; suivant : 001646In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease.
Auteurs : C S Lee [Canada] ; 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 StoesslSource :
- Annals of neurology [ 0364-5134 ] ; 2000.
English descriptors
- KwdEn :
- Aged, Carbon Radioisotopes, Carrier Proteins (metabolism), Corpus Striatum (diagnostic imaging), Corpus Striatum (metabolism), Dopamine (metabolism), Dopamine Plasma Membrane Transport Proteins, Down-Regulation (physiology), Fluorine Radioisotopes, Homovanillic Acid (metabolism), Humans, Membrane Glycoproteins, Membrane Transport Proteins, Middle Aged, Nerve Tissue Proteins, Parkinson Disease (diagnostic imaging), Parkinson Disease (metabolism), Presynaptic Terminals (metabolism), Tetrabenazine (analogs & derivatives), Tomography, Emission-Computed.
- MESH :
- chemical , analogs & derivatives : Tetrabenazine.
- chemical , metabolism : Carrier Proteins, Dopamine, Homovanillic Acid.
- chemical : Carbon Radioisotopes, Dopamine Plasma Membrane Transport Proteins, Fluorine Radioisotopes, Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins.
- diagnostic imaging : Corpus Striatum, Parkinson Disease.
- metabolism : Corpus Striatum, Parkinson Disease, Presynaptic Terminals.
- physiology : Down-Regulation.
- Aged, Humans, Middle Aged, Tomography, Emission-Computed.
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 [11C]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 [11]DTBZ, and of [11C]methylphenidate and [11C]DTBZ, were compared between the PD and the normal control subjects. We found that [18F]dopa Ki was reduced less than the binding potential (Bmax/Kd) for [11C]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.
PubMed: 10762161
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pubmed:10762161Le document en format XML
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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 [11C]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 [11]DTBZ, and of [11C]methylphenidate and [11C]DTBZ, were compared between the PD and the normal control subjects. We found that [18F]dopa Ki was reduced less than the binding potential (Bmax/Kd) for [11C]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.</div>
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<Abstract><AbstractText>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 [11C]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 [11]DTBZ, and of [11C]methylphenidate and [11C]DTBZ, were compared between the PD and the normal control subjects. We found that [18F]dopa Ki was reduced less than the binding potential (Bmax/Kd) for [11C]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.</AbstractText>
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