Dopamine transporter relation to dopamine turnover in Parkinson's disease: a positron emission tomography study.
Identifieur interne : 001035 ( PubMed/Corpus ); précédent : 001034; suivant : 001036Dopamine transporter relation to dopamine turnover in Parkinson's disease: a positron emission tomography study.
Auteurs : Vesna Sossi ; Raúl De La Fuente-Fernández ; Michael Schulzer ; Andre R. Troiano ; Thomas J. Ruth ; A Jon StoesslSource :
- Annals of neurology [ 1531-8249 ] ; 2007.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine, Dopamine Plasma Membrane Transport Proteins.
- diagnosis : Parkinson Disease.
- metabolism : Parkinson Disease, Presynaptic Terminals.
- methods : Positron-Emission Tomography.
- physiology : Protein Binding.
- Aged, Female, Humans, Male, Middle Aged.
Abstract
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.
DOI: 10.1002/ana.21204
PubMed: 17886297
Links to Exploration step
pubmed:17886297Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dopamine transporter relation to dopamine turnover in Parkinson's disease: a positron emission tomography study.</title><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><affiliation><nlm:affiliation>University of British Columbia, Vancouver, British Columbia, Canada. vesna@physics.ubc.ca</nlm:affiliation></affiliation></author><author><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name></author><author><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name></author><author><name sortKey="Troiano, Andre R" sort="Troiano, Andre R" uniqKey="Troiano A" first="Andre R" last="Troiano">Andre R. Troiano</name></author><author><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</name></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17886297</idno><idno type="pmid">17886297</idno><idno type="doi">10.1002/ana.21204</idno><idno type="wicri:Area/PubMed/Corpus">001035</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001035</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dopamine transporter relation to dopamine turnover in Parkinson's disease: a positron emission tomography study.</title><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><affiliation><nlm:affiliation>University of British Columbia, Vancouver, British Columbia, Canada. vesna@physics.ubc.ca</nlm:affiliation></affiliation></author><author><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name></author><author><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name></author><author><name sortKey="Troiano, Andre R" sort="Troiano, Andre R" uniqKey="Troiano A" first="Andre R" last="Troiano">Andre R. Troiano</name></author><author><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</name></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></author></analytic><series><title level="j">Annals of neurology</title><idno type="eISSN">1531-8249</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (metabolism)</term><term>Positron-Emission Tomography (methods)</term><term>Presynaptic Terminals (metabolism)</term><term>Protein Binding (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Dopamine Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term><term>Presynaptic Terminals</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Positron-Emission Tomography</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Protein Binding</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17886297</PMID><DateCreated><Year>2007</Year><Month>12</Month><Day>06</Day></DateCreated><DateCompleted><Year>2007</Year><Month>12</Month><Day>27</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8249</ISSN><JournalIssue CitedMedium="Internet"><Volume>62</Volume><Issue>5</Issue><PubDate><Year>2007</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Annals of neurology</Title><ISOAbbreviation>Ann. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Dopamine transporter relation to dopamine turnover in Parkinson's disease: a positron emission tomography study.</ArticleTitle><Pagination><MedlinePgn>468-74</MedlinePgn></Pagination><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="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.</AbstractText><AbstractText Label="METHODS" NlmCategory="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 (11)C-methylphenidate (MP, a DAT marker), (11)C-dihydrotetrabenazine (a vesicular monoamine transporter 2 marker), and (18)F-fluorodopa, leading to the determination of the MP and (11)C-dihydrotetrabenazine binding potentials (BPs) and the effective distribution volume for (18)F-fluorodopa, the inverse of DA turnover. Seven patients also underwent positron emission tomography with (11)C-raclopride before and 1 hour after levodopa administration to estimate levodopa-induced changes in synaptic DA concentration.</AbstractText><AbstractText Label="RESULTS" NlmCategory="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.</AbstractText><AbstractText Label="INTERPRETATION" NlmCategory="CONCLUSIONS">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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sossi</LastName><ForeName>Vesna</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>University of British Columbia, Vancouver, British Columbia, Canada. vesna@physics.ubc.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de la Fuente-Fernández</LastName><ForeName>Raúl</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Schulzer</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Troiano</LastName><ForeName>Andre R</ForeName><Initials>AR</Initials></Author><Author ValidYN="Y"><LastName>Ruth</LastName><ForeName>Thomas J</ForeName><Initials>TJ</Initials></Author><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A Jon</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><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="D050483">Dopamine Plasma Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></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><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049268" MajorTopicYN="Y">Positron-Emission Tomography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017729" MajorTopicYN="N">Presynaptic Terminals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>9</Month><Day>22</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>12</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>9</Month><Day>22</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17886297</ArticleId><ArticleId IdType="doi">10.1002/ana.21204</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001035 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001035 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:17886297
|texte= Dopamine transporter relation to dopamine turnover in Parkinson's disease: a positron emission tomography study.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:17886297" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonCanadaV1
| This area was generated with Dilib version V0.6.29. |  |