JNM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH RSS TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


First published online July 17, 2009, 10.2967/jnumed.109.063529
This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jnumed.109.063529v1
50/8/1244    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in JNM
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ribeiro, M.-J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ribeiro, M.-J.
Journal of Nuclear Medicine Vol. 50 No. 8 1244-1250
© 2009 by Society of Nuclear Medicine

doi: 10.2967/jnumed.109.063529

Clinical Investigation

A Multitracer Dopaminergic PET Study of Young-Onset Parkinsonian Patients With and Without Parkin Gene Mutations

Maria-João Ribeiro1, Stéphane Thobois2, Ebba Lohmann3–5, Sophie Tezenas du Montcel6,7, Suzanne Lesage3,5, Antoine Pelissolo8, Bruno Dubois3,5,9, Luc Mallet10, Pierre Pollak11, Yves Agid3–512, Emmanuel Broussolle2, Alexis Brice3–513, Philippe Remy14,15 and and The French Parkinson's Disease Genetics Study Group

1 CEA, I2BM, Service Hospitalier Frédéric Joliot, Orsay, France; 2 University of Lyon; Hospices Civils de Lyon, Neurological Hospital, Lyon, France; 3 INSERM, Paris, France; 4 Department of the Nervous System Disorders, AP-HP, Pitié-Salpêtrière Hospital, Paris, France; 5 UPMC University of Paris, Paris, France; 6 Unit of de Biostatistics and Medical Information and Unit of Medical Research, AP-HP, Pitié-Salpêtrière Hospital, Paris, France; 7 Modelisation in Clinical Research, UPMC University of Paris, Paris, France; 8 Department of Psychiatry, AP-HP, Pitié-Salpêtrière Hospital, Paris, France; 9 Centre de Référence sur la Maladie de Pick, AP-HP, Pitié-Salpêtrière Hospital, Paris, France; 10 Behaviour, Emotion and Basal Ganglia, Center of Clinical Investigation, INSERM Avenir Group, Paris, France; 11 Department of Clinical and Biological Neurosciences, University Hospital of Grenoble, Grenoble, France; 12 Clinical Investigation Center, AP-HP, Pitié-Salpêtrière Hospital, Paris, France; 13 Department of Genetics and Cytogenetics, AP-HP, Pitié-Salpêtrière Hospital, Paris, France; 14 CEA, I2BM, MIRCEN, URA CEA-CNRS 2210, Orsay, France; and 15 CHU Henri Mondor, AP-HP and Faculté de Médecine Paris 12, Créteil, France

Correspondence: For correspondence or reprints contact: Maria João Ribeiro, Service Hospitalier Frédéric Joliot, I2BM/DSV, CEA, 4, Place du Général Leclerc, F-91406 Orsay, France. E-mail: maria-joao.ribeiro{at}cea.fr

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 18F-fluoro-L-3,4-dihydroxyphenylalanine (18F-fluoro-L-DOPA), 11C-PE2I, and 11C-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. Methods: A total of 35 YOPD patients were enrolled (16 with parkin mutation, 19 without). The uptake constant (Ki) of 18F-fluoro-L-DOPA and the binding potential (BP) of 11C-PE2I (BPDAT) and of 11C-raclopride (BPD2) 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. Results: In YOPD patients, 18F-fluoro-L-DOPA Ki 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 Ki values and cognitive or motor status. 11C-PE2I BPDAT 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 11C-raclopride BPD2 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 11C-raclopride in the frontal cortex and a decrease of 18F-fluoro-L-DOPA and 11C-PE2I uptake in the substantia nigra bilaterally (P < 0.05, false-discovery rate–corrected). Conclusion: Carriers of parkin mutations are indistinguishable on PET markers of dopaminergic dysfunction from other YOPD patients with long disease duration.

Key Words: Parkinson • parkin gene • PET • 18F-fluoro-L-DOPA • 11C-PE2I • 11C-raclopride

COPYRIGHT © 2009 by the Society of Nuclear Medicine, Inc.


Related articles in JNM:

This Month in JNM

JNM 2009 50: 11A-12A. [Full Text]  






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH RSS TABLE OF CONTENTS
JOURNAL OF NUCLEAR MEDICINE TECHNOLOGY THE JOURNAL OF NUCLEAR MEDICINE
Copyright © 2009 by the Society of Nuclear Medicine.