Long-term changes of striatal dopamine D2 receptors in patients with Parkinson's disease: a study with positron emission tomography and [11C]raclopride.
Identifieur interne : 004735 ( PubMed/Curation ); précédent : 004734; suivant : 004736Long-term changes of striatal dopamine D2 receptors in patients with Parkinson's disease: a study with positron emission tomography and [11C]raclopride.
Auteurs : A. Antonini [Suisse] ; J. Schwarz ; W H Oertel ; O. Pogarell ; K L LeendersSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1997.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (therapeutic use), Caudate Nucleus (drug effects), Caudate Nucleus (physiopathology), Caudate Nucleus (radionuclide imaging), Corpus Striatum (drug effects), Corpus Striatum (physiopathology), Corpus Striatum (radionuclide imaging), Dopamine Agonists (therapeutic use), Dopamine Antagonists (pharmacokinetics), Drug Therapy, Combination, Female, Follow-Up Studies, Humans, Levodopa (therapeutic use), Longitudinal Studies, Male, Middle Aged, Neural Pathways (drug effects), Neural Pathways (physiopathology), Neural Pathways (radionuclide imaging), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson Disease (radionuclide imaging), Putamen (drug effects), Putamen (physiopathology), Putamen (radionuclide imaging), Raclopride, Receptors, Dopamine D2 (drug effects), Receptors, Dopamine D2 (physiology), Salicylamides (pharmacokinetics), Substantia Nigra (drug effects), Substantia Nigra (physiopathology), Substantia Nigra (radionuclide imaging), Tomography, Emission-Computed.
- MESH :
- chemical , drug effects : Receptors, Dopamine D2.
- chemical , pharmacokinetics : Dopamine Antagonists, Salicylamides.
- chemical , physiology : Receptors, Dopamine D2.
- chemical , therapeutic use : Antiparkinson Agents, Dopamine Agonists, Levodopa.
- drug effects : Caudate Nucleus, Corpus Striatum, Neural Pathways, Putamen, Substantia Nigra.
- drug therapy : Parkinson Disease.
- physiopathology : Caudate Nucleus, Corpus Striatum, Neural Pathways, Parkinson Disease, Putamen, Substantia Nigra.
- radionuclide imaging : Caudate Nucleus, Corpus Striatum, Neural Pathways, Parkinson Disease, Putamen, Substantia Nigra.
- Aged, Drug Therapy, Combination, Female, Follow-Up Studies, Humans, Longitudinal Studies, Male, Middle Aged, Raclopride, Tomography, Emission-Computed.
Abstract
We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug-naive stage and 3-5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3-5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at "off" had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3-4 months after therapy began and that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long-term downregulation of striatal dopamine D2 receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.
DOI: 10.1002/mds.870120107
PubMed: 8990051
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Antonini</name><affiliation wicri:level="1"><nlm:affiliation>PET Department, Paul Scherrer Institute, Villigen, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>PET Department, Paul Scherrer Institute, Villigen</wicri:regionArea></affiliation></author><author><name sortKey="Schwarz, J" sort="Schwarz, J" uniqKey="Schwarz J" first="J" last="Schwarz">J. Schwarz</name></author><author><name sortKey="Oertel, W H" sort="Oertel, W H" uniqKey="Oertel W" first="W H" last="Oertel">W H Oertel</name></author><author><name sortKey="Pogarell, O" sort="Pogarell, O" uniqKey="Pogarell O" first="O" last="Pogarell">O. Pogarell</name></author><author><name sortKey="Leenders, K L" sort="Leenders, K L" uniqKey="Leenders K" first="K L" last="Leenders">K L Leenders</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antiparkinson Agents (therapeutic use)</term><term>Caudate Nucleus (drug effects)</term><term>Caudate Nucleus (physiopathology)</term><term>Caudate Nucleus (radionuclide imaging)</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (physiopathology)</term><term>Corpus Striatum (radionuclide imaging)</term><term>Dopamine Agonists (therapeutic use)</term><term>Dopamine Antagonists (pharmacokinetics)</term><term>Drug Therapy, Combination</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Neural Pathways (drug effects)</term><term>Neural Pathways (physiopathology)</term><term>Neural Pathways (radionuclide imaging)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Putamen (drug effects)</term><term>Putamen (physiopathology)</term><term>Putamen (radionuclide imaging)</term><term>Raclopride</term><term>Receptors, Dopamine D2 (drug effects)</term><term>Receptors, Dopamine D2 (physiology)</term><term>Salicylamides (pharmacokinetics)</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (physiopathology)</term><term>Substantia Nigra (radionuclide imaging)</term><term>Tomography, Emission-Computed</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Dopamine Antagonists</term><term>Salicylamides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agonists</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Neural Pathways</term><term>Putamen</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Neural Pathways</term><term>Parkinson Disease</term><term>Putamen</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Neural Pathways</term><term>Parkinson Disease</term><term>Putamen</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Drug Therapy, Combination</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Raclopride</term><term>Tomography, Emission-Computed</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug-naive stage and 3-5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3-5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at "off" had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3-4 months after therapy began and that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long-term downregulation of striatal dopamine D2 receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">8990051</PMID><DateCreated><Year>1997</Year><Month>04</Month><Day>02</Day></DateCreated><DateCompleted><Year>1997</Year><Month>04</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>12</Volume><Issue>1</Issue><PubDate><Year>1997</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Long-term changes of striatal dopamine D2 receptors in patients with Parkinson's disease: a study with positron emission tomography and [11C]raclopride.</ArticleTitle><Pagination><MedlinePgn>33-8</MedlinePgn></Pagination><Abstract><AbstractText>We used [11C]raclopride (RACLO) and positron emission tomography (PET) to study longitudinally striatal dopamine D2 receptor binding in nine patients with Parkinson's disease (PD) at an early drug-naive stage and 3-5 years later, when motor fluctuations had appeared in seven of them. Patients were treated with a combination of levodopa and dopamine agonists. Data were compared with 10 healthy controls in the same age range. Initially, patients with PD showed a significant increase of RACLO uptake in the putamen compared with controls (p < 0.04). The caudate nucleus revealed values in the normal range. After 3-5 years, RACLO binding was significantly reduced in the putamen (p < 0.03) and caudate nucleus (p < 0.03) compared with baseline. Values were now in the control range in the putamen and reduced in the caudate nucleus (p < 0.05). The clinical score at "off" had significantly worsened (p < 0.0005) compared with the first PET scan. The nine PD patients reported here had already been investigated 3-4 months after therapy began and that time did not show a reduction of the initially increased RACLO binding capacity (data published previously). These results indicate long-term downregulation of striatal dopamine D2 receptor binding in PD. Receptor changes in the striatum of patients with PD may be induced by chronic dopaminergic therapy or occur independently of treatment, as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of nigrostriatal neurons.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Antonini</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>PET Department, Paul Scherrer Institute, Villigen, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schwarz</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Oertel</LastName><ForeName>W H</ForeName><Initials>WH</Initials></Author><Author ValidYN="Y"><LastName>Pogarell</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Leenders</LastName><ForeName>K L</ForeName><Initials>KL</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018491">Dopamine Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018492">Dopamine Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017448">Receptors, Dopamine D2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012457">Salicylamides</NameOfSubstance></Chemical><Chemical><RegistryNumber>430K3SOZ7G</RegistryNumber><NameOfSubstance UI="D020891">Raclopride</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002421">Caudate Nucleus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003342">Corpus Striatum</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018491">Dopamine Agonists</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018492">Dopamine Antagonists</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000493">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004359">Drug Therapy, Combination</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005500">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008137">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009434">Neural Pathways</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011699">Putamen</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020891">Raclopride</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017448">Receptors, Dopamine D2</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012457">Salicylamides</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000493">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013378">Substantia Nigra</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D014055">Tomography, Emission-Computed</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8990051</ArticleId><ArticleId IdType="doi">10.1002/mds.870120107</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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