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Dopaminergic Function and Dopamine Transporter Binding Assessed With Positron Emission Tomography in Parkinson Disease
Maria-Joao Ribeiro, MD, PhD;
Marie Vidailhet, MD;
Christian Loc'h, BS;
Corinne Dupel, MD;
Jean Paul Nguyen, MD;
Michel Ponchant, BS;
Frédéric Dollé, PhD;
Marc Peschanski, MD, PhD;
Philippe Hantraye, PhD;
Pierre Cesaro, MD, PhD;
Yves Samson, MD;
Philippe Remy, MD, PhD
Arch Neurol. 2002;59:580-586.
Background Measuring progression of Parkinson disease (PD) using positron emission
tomography may help demonstrate the efficacy of neuroprotective treatments.
To date, 18F-dopa has been the gold standard to measure presynaptic
dopaminergic function in PD, but this tracer might overestimate the rate of
neuronal death in PD because its uptake also depends on dopamine turnover
rather than exclusively on the density of dopaminergic terminals in the striatum.
The latter might be assessed using newly developed ligands of the membrane
dopamine transporter.
Objective To compare the striatal uptakes of 18F-dopa and 76Br-FE-CBT,
a dopamine transporter ligand, in patients with PD.
Patients and Methods The striatal uptakes of 76Br-FE-CBT and 18F-dopa
were compared using positron emission tomography in 10 patients with early
PD and 8 with advanced PD. Correlation of uptakes with motor performance was
investigated.
Results The reduction in 76Br-FE-CBT binding to 43% of control values
was more severe than the reduction in 18F-dopa uptake (63% of control
values) in the putamen of patients with early PD. No significant difference
was found between either tracer's uptake in the putamen of patients with advanced
PD. Motor performance was highly correlated to 18F-dopa uptake,
whereas correlation to 76Br-FE-CBT binding was weak.
Conclusions Uptake of 18F-dopa may be up-regulated in early PD, suggesting
a compensatory increase of dopamine synthesis in surviving dopaminergic terminals.
Positron emission tomography dopamine transporter ligands and 18F-dopa
give complementary information on the presynaptic status of the nigrostriatal
dopaminergic system and might be associated to investigate the efficacy of
neuroprotective treatments in PD.
From Commissariat à l'Energie Atomique (CEA), Service Hospitalier
Frédéric Joliot, Orsay, France (Drs Ribeiro, Dupel, Dollé,
Samson, and Remy and Messrs Loc'h and Ponchant); Service de Neurologie, Hôpital
Saint-Antoine, Paris, France (Dr Vidailhet); Institut National de la Santé
et de la Recherche Médicale (INSERM) U289, Paris (Dr Vidailhet); Département
de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, Assistance
Publique-Hôpitaux de Paris & Université Paris 12, Créteil,
France (Drs Nguyen, Peschanski, Cesaro, and Remy); INSERM U421, IM3, Faculté
de Médecine, Créteil (Drs Nguyen, Peschanski, and Cesaro); Unité
de Recherche Associée CEACentre National de la Recherche Scientifique
2210, Orsay (Drs Hantraye and Remy); and Urgences Cérébro-Vasculaires,
CHU Pitié-Salpétrière, Paris (Dr Samson)
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