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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Sossi</name></author><author><name sortKey="Ruth, T J" sort="Ruth, T J" uniqKey="Ruth T" first="T J" last="Ruth">T J Ruth</name></author><author><name sortKey="Schulzer, M" sort="Schulzer, M" uniqKey="Schulzer M" first="M" last="Schulzer">M. Schulzer</name></author><author><name sortKey="Holden, J E" sort="Holden, J E" uniqKey="Holden J" first="J E" last="Holden">J E Holden</name></author><author><name sortKey="Wudel, J" sort="Wudel, J" uniqKey="Wudel J" first="J" last="Wudel">J. Wudel</name></author><author><name sortKey="Pal, P K" sort="Pal, P K" uniqKey="Pal P" first="P K" last="Pal">P K Pal</name></author><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. 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Samii</name></author><author><name sortKey="Sossi, V" sort="Sossi, V" uniqKey="Sossi V" first="V" last="Sossi">V. Sossi</name></author><author><name sortKey="Ruth, T J" sort="Ruth, T J" uniqKey="Ruth T" first="T J" last="Ruth">T J Ruth</name></author><author><name sortKey="Schulzer, M" sort="Schulzer, M" uniqKey="Schulzer M" first="M" last="Schulzer">M. Schulzer</name></author><author><name sortKey="Holden, J E" sort="Holden, J E" uniqKey="Holden J" first="J E" last="Holden">J E Holden</name></author><author><name sortKey="Wudel, J" sort="Wudel, J" uniqKey="Wudel J" first="J" last="Wudel">J. Wudel</name></author><author><name sortKey="Pal, P K" sort="Pal, P K" uniqKey="Pal P" first="P K" last="Pal">P K Pal</name></author><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></author><author><name sortKey="Calne, D B" sort="Calne, D B" uniqKey="Calne D" first="D B" last="Calne">D B Calne</name></author><author><name sortKey="Stoessl, A J" sort="Stoessl, A J" uniqKey="Stoessl A" first="A J" last="Stoessl">A J Stoessl</name></author></analytic><series><title level="j">Annals of neurology</title><idno type="ISSN">0364-5134</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Carbon Radioisotopes</term><term>Carrier Proteins (metabolism)</term><term>Corpus Striatum (diagnostic imaging)</term><term>Corpus Striatum (metabolism)</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Down-Regulation (physiology)</term><term>Fluorine Radioisotopes</term><term>Homovanillic Acid (metabolism)</term><term>Humans</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Middle Aged</term><term>Nerve Tissue Proteins</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (metabolism)</term><term>Presynaptic Terminals (metabolism)</term><term>Tetrabenazine (analogs & derivatives)</term><term>Tomography, Emission-Computed</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tetrabenazine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term><term>Dopamine</term><term>Homovanillic Acid</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Carbon Radioisotopes</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Fluorine Radioisotopes</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Presynaptic Terminals</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Down-Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Humans</term><term>Middle Aged</term><term>Tomography, Emission-Computed</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10762161</PMID><DateCreated><Year>2000</Year><Month>04</Month><Day>21</Day></DateCreated><DateCompleted><Year>2000</Year><Month>04</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0364-5134</ISSN><JournalIssue CitedMedium="Print"><Volume>47</Volume><Issue>4</Issue><PubDate><Year>2000</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Annals of neurology</Title><ISOAbbreviation>Ann. Neurol.</ISOAbbreviation></Journal><ArticleTitle>In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>493-503</MedlinePgn></Pagination><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></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>C S</ForeName><Initials>CS</Initials><AffiliationInfo><Affiliation>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, British Columbia, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Samii</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Sossi</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Ruth</LastName><ForeName>T J</ForeName><Initials>TJ</Initials></Author><Author ValidYN="Y"><LastName>Schulzer</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Holden</LastName><ForeName>J E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Wudel</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Pal</LastName><ForeName>P K</ForeName><Initials>PK</Initials></Author><Author ValidYN="Y"><LastName>de la Fuente-Fernandez</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Calne</LastName><ForeName>D B</ForeName><Initials>DB</Initials></Author><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Ann Neurol</MedlineTA><NlmUniqueID>7707449</NlmUniqueID><ISSNLinking>0364-5134</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002250">Carbon Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050483">Dopamine Plasma Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005462">Fluorine Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>3466-75-9</RegistryNumber><NameOfSubstance UI="C032811">dihydrotetrabenazine</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>X77S6GMS36</RegistryNumber><NameOfSubstance UI="D006719">Homovanillic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>Z9O08YRN8O</RegistryNumber><NameOfSubstance UI="D013747">Tetrabenazine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002250" MajorTopicYN="N">Carbon Radioisotopes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050483" MajorTopicYN="N">Dopamine Plasma Membrane Transport Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005462" MajorTopicYN="N">Fluorine Radioisotopes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006719" MajorTopicYN="N">Homovanillic Acid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008562" MajorTopicYN="Y">Membrane Glycoproteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D026901" MajorTopicYN="Y">Membrane Transport Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009419" MajorTopicYN="Y">Nerve Tissue Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017729" MajorTopicYN="N">Presynaptic Terminals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013747" MajorTopicYN="N">Tetrabenazine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014055" MajorTopicYN="Y">Tomography, Emission-Computed</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>4</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>4</Month><Day>29</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>4</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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