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Neurology 2000;55:877-879
© 2000 American Academy of Neurology
Brief Communications

[18F]-dopa PET study in patients with juvenile-onset PD and parkin gene mutations

E. Broussolle, MD, C. B. Lücking, MD, N. Ginovart, PhD, P. Pollak, MD, P. Remy, MD, PhD, A. Dürr, MD and The French Parkinson’s Disease Genetics Study Group*

From the Department of Neurology (Dr. Broussolle), and CERMEP Cyclotron Unit (Drs. Broussolle and Ginovart), Hôpital Neurologique Pierre Wertheimer, Lyon; INSERM U 289 (Drs. Lücking and Dürr), Hôpital de la Salpêtrière, Paris; Department of Clinical and Biological Neurosciences (Dr. Pollak), Hôpital Nord, Grenoble; and Service Hospitalier Frédéric Joliot (Dr. Remy), Orsay, France.

Address correspondence and reprint requests to Dr. Emmanuel Broussolle, Service de Neurologie D, Hôpital Neurologique Pierre Wertheimer, 59 boulevard Pinel, 69003, Lyon, France.

Article abstract—Parkin gene mutations cause a form of early-onset autosomal recessive PD with neuronal loss in the substantia nigra and no Lewy bodies. The authors present a PET [18F]-dopa study of one familial and two sporadic cases with juvenile-onset PD resulting from parkin gene mutations. They found a profound decrease of [18F]-dopa uptake, representing 28% of putamen and 44% of caudate nucleus control subject values. PD caused by parkin gene mutations is distinct from idiopathic PD on molecular grounds but has similar clinical and PET findings.




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