Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington's disease

• DOI: 10.1093/brain/119.6.2085
• Publication Date: 2007-01-13T16:54:21Z
• Authors: A. Antonini; K. L. Leenders; R. Spiegel; D. Meier; P. Vontobel; M. Weigell-Weber; R. Sanchez-Pernaute; J. G. de Yébenez; P. Boesiger; A. Weindl; R. P. Maguire
• Keywords: Putamen; Caudate nucleus; Asymptomatic carrier

We used PET scans with the tracers [18F]fluorodeoxyglucose (FDG) and [11C]raclopride (RACLO) to study glucose metabolism dopamine D2 receptor binding in caudate nucleus putamen of 18 carriers Huntington's disease gene mutation (10 asymptomatic subjects eight untreated symptomatic patients an early stage). also performed MR1 measured bicaudate ratio (BCR) same subjects. Data were compared those from nine mutation-negative members families separate groups age matched controls. The repeated 1.5–3 years later six carriers. Symptomatic showed a marked reduction FDG RACLO uptake significant increase BCR. Asymptomatic revealed hypometabolism putamen. was significantly decreased Decrements tracer uptake, particularly RACLO, correlated BCR increases both In carriers, metabolic decreases associated CAG repeat number but not individual's age. Discriminant function analysis correctly classified clinical genetic status 24 27 on basis their striatal values (83% sensitivity 100% specificity). Three classified/grouped together subjects, indicating that these individuals had normal uptake. Follow-up data gene-positive mean 6.3% per year. Striatal overall non 2.3% decrease year These indicate may show neuronal for long period life. findings suggest it be possible predict when carrier will develop symptoms serial measurements function.