A multitracer dopaminergic PET study of young-onset parkinsonian patients with and without parkin gene mutations.
Identifieur interne : 000B70 ( PubMed/Corpus ); précédent : 000B69; suivant : 000B71A multitracer dopaminergic PET study of young-onset parkinsonian patients with and without parkin gene mutations.
Auteurs : Maria-João Ribeiro ; Stéphane Thobois ; Ebba Lohmann ; Sophie Tezenas Du Montcel ; Suzanne Lesage ; Antoine Pelissolo ; Bruno Dubois ; Luc Mallet ; Pierre Pollak ; Yves Agid ; Emmanuel Broussolle ; Alexis Brice ; Philippe RemySource :
- Journal of nuclear medicine : official publication, Society of Nuclear Medicine [ 0161-5505 ] ; 2009.
English descriptors
- KwdEn :
- Brain (diagnostic imaging), Brain (metabolism), Female, Heterozygote, Humans, Male, Middle Aged, Mutation (genetics), Parkinsonian Disorders (diagnostic imaging), Parkinsonian Disorders (genetics), Parkinsonian Disorders (metabolism), Radioisotopes (pharmacokinetics), Radionuclide Imaging, Radiopharmaceuticals (pharmacokinetics), Receptors, Dopamine (metabolism), Tissue Distribution, Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , genetics : Ubiquitin-Protein Ligases.
- chemical , metabolism : Receptors, Dopamine.
- chemical , pharmacokinetics : Radioisotopes, Radiopharmaceuticals.
- diagnostic imaging : Brain, Parkinsonian Disorders.
- genetics : Mutation, Parkinsonian Disorders.
- metabolism : Brain, Parkinsonian Disorders.
- Female, Heterozygote, Humans, Male, Middle Aged, Radionuclide Imaging, Tissue Distribution.
Abstract
The impact of parkin gene mutations on nigrostriatal dopaminergic degeneration is not well established. The purpose of this study was to characterize by PET using (18)F-fluoro-l-3,4-dihydroxyphenylalanine ((18)F-fluoro-l-DOPA), (11)C-PE2I, and (11)C-raclopride the pattern of dopaminergic lesions in young-onset Parkinson disease (YOPD) patients with or without mutations of the parkin gene and to correlate the clinical and neuropsychologic characteristics of these patients with PET results.
DOI: 10.2967/jnumed.109.063529
PubMed: 19617340
Links to Exploration step
pubmed:19617340Le document en format XML
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<author><name sortKey="Ribeiro, Maria Joao" sort="Ribeiro, Maria Joao" uniqKey="Ribeiro M" first="Maria-João" last="Ribeiro">Maria-João Ribeiro</name>
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<author><name sortKey="Thobois, Stephane" sort="Thobois, Stephane" uniqKey="Thobois S" first="Stéphane" last="Thobois">Stéphane Thobois</name>
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<author><name sortKey="Lesage, Suzanne" sort="Lesage, Suzanne" uniqKey="Lesage S" first="Suzanne" last="Lesage">Suzanne Lesage</name>
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<author><name sortKey="Mallet, Luc" sort="Mallet, Luc" uniqKey="Mallet L" first="Luc" last="Mallet">Luc Mallet</name>
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<author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name>
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<front><div type="abstract" xml:lang="en">The impact of parkin gene mutations on nigrostriatal dopaminergic degeneration is not well established. The purpose of this study was to characterize by PET using (18)F-fluoro-l-3,4-dihydroxyphenylalanine ((18)F-fluoro-l-DOPA), (11)C-PE2I, and (11)C-raclopride the pattern of dopaminergic lesions in young-onset Parkinson disease (YOPD) patients with or without mutations of the parkin gene and to correlate the clinical and neuropsychologic characteristics of these patients with PET results.</div>
</front>
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<DateCreated><Year>2009</Year>
<Month>08</Month>
<Day>04</Day>
</DateCreated>
<DateCompleted><Year>2009</Year>
<Month>09</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>11</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0161-5505</ISSN>
<JournalIssue CitedMedium="Print"><Volume>50</Volume>
<Issue>8</Issue>
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<Month>Aug</Month>
</PubDate>
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<Title>Journal of nuclear medicine : official publication, Society of Nuclear Medicine</Title>
<ISOAbbreviation>J. Nucl. Med.</ISOAbbreviation>
</Journal>
<ArticleTitle>A multitracer dopaminergic PET study of young-onset parkinsonian patients with and without parkin gene mutations.</ArticleTitle>
<Pagination><MedlinePgn>1244-50</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.2967/jnumed.109.063529</ELocationID>
<Abstract><AbstractText Label="UNLABELLED">The impact of parkin gene mutations on nigrostriatal dopaminergic degeneration is not well established. The purpose of this study was to characterize by PET using (18)F-fluoro-l-3,4-dihydroxyphenylalanine ((18)F-fluoro-l-DOPA), (11)C-PE2I, and (11)C-raclopride the pattern of dopaminergic lesions in young-onset Parkinson disease (YOPD) patients with or without mutations of the parkin gene and to correlate the clinical and neuropsychologic characteristics of these patients with PET results.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">A total of 35 YOPD patients were enrolled (16 with parkin mutation, 19 without). The uptake constant (K(i)) of (18)F-fluoro-l-DOPA and the binding potential (BP) of (11)C-PE2I (BP(DAT)) and of (11)C-raclopride (BP(D2)) were calculated in the striatum. Comparisons were made between the 2 groups of YOPD and between controls and patients. For each radiotracer, parametric images were obtained, and statistical parametric mapping (SPM) analysis using a voxel-by-voxel statistical t test was performed. Correlations between the cognitive and motor status and PET results were analyzed.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">In YOPD patients, (18)F-fluoro-l-DOPA K(i) values were reduced to 68% (caudate) and 40% (putamen) of normal values (P < 0.0001). This decrease was symmetric and comparable for nonparkin and parkin patients. No correlation was found between the K(i) values and cognitive or motor status. (11)C-PE2I BP(DAT) values in YOPD patients were decreased to 56% (caudate) and 41% (putamen) of normal values (P < 0.0001) and did not differ between the 2 YOPD populations. The mean (11)C-raclopride BP(D2) values were reduced to 72% (caudate) and 84% (putamen) of the normal values (P < 0.02) and did not differ between nonparkin and parkin patients. SPM analyses showed in patients an additional decrease of (11)C-raclopride in the frontal cortex and a decrease of (18)F-fluoro-l-DOPA and (11)C-PE2I uptake in the substantia nigra bilaterally (P < 0.05, false-discovery rate-corrected).</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Carriers of parkin mutations are indistinguishable on PET markers of dopaminergic dysfunction from other YOPD patients with long disease duration.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ribeiro</LastName>
<ForeName>Maria-João</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo><Affiliation>CEA, I2BM, Service Hospitalier Frédéric Joliot, Orsay, France. maria-joao.ribeiro@cea.fr</Affiliation>
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<Author ValidYN="Y"><LastName>Thobois</LastName>
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<Author ValidYN="Y"><LastName>Lohmann</LastName>
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<Author ValidYN="Y"><LastName>du Montcel</LastName>
<ForeName>Sophie Tezenas</ForeName>
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<Author ValidYN="Y"><LastName>Lesage</LastName>
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<Author ValidYN="Y"><LastName>Pelissolo</LastName>
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<Author ValidYN="Y"><LastName>Dubois</LastName>
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<Author ValidYN="Y"><LastName>Brice</LastName>
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</Author>
<Author ValidYN="Y"><LastName>Remy</LastName>
<ForeName>Philippe</ForeName>
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<Author ValidYN="Y"><CollectiveName>French Parkinson's Disease Genetics Study Group</CollectiveName>
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