In vivo tau PET imaging using [11C]PBB3 in patients with PSP and CBS

Objective: To investigate characteristics of [11C]PBB3 binding andits relation with clinical aspects in patients with progressivesupranuclear palsy (PSP) and corticobasal syndrome (CBS).Background: [11C]PBB3 is a novel tau imaging positron emissiontomography (PET) ligand, which could visualize the tau deposition inAlzheimer’s disease (AD) and non-AD tauopathies such as PSP,CBS and frontotemporal dementia.Methods: Participants included 10 PSP patients, 9 patients withcorticobasal syndrome (CBS), 19 AD patients, and 20 age andgender matched healthy controls (HCs). A dose (about 10 mCi) of[11C]PBB3 was intravenously injected and sequential PET scanswere performed for 70 min. We also performed PET scan with aplaque-binding agent, [11C]PIB (about 10 mCi), for 70 min and threedimensionalT1-weighted MRI. Standardized uptake value ratio(SUVR) was calculated for each PET image using the cerebellarcortex as reference region. Amyloid deposition was verified by visualassessment of SUVR images of [11C]PIB PET. As for [11C]PBB3PET data, group analysis among each group was performed by onewayANOVA using statistical parametric mapping software (spm5).Results: One CBS patient and 17 of 19 AD patients were PIBpositive,and all the rest participants were PIB-negative. One PIBpositiveCBS and two PIB-negative AD patients were excluded fromgroup analysis. [11C]PBB3 was accumulated in lesions associatedwith neurological symptoms in PSP, CBS and AD patients. To bespecific, [11C]PBB3 binding was significantly increased in thebrainstem, basal ganglia, thalamus and dentate nucleus in PSPpatients compared to HCs. In PIB-negative CBS patients,remarkable uptake of [11C]PBB3 was observed in basal ganglia andthe neocortex including the supplementary motor area (SMA) andthe peri-Rolandic area compared to HCs. Furthermore, [11C]PBB3retention observed in PIB-positive CBS patient extended theneocortex as well as the entire limbic system, resembling ADpatients with profound cognitive decline. Some brain lesions with[11C]PBB3 binding exhibited brain atrophy in PSP, CBS and ADpatients.Conclusions: The present study demonstrated that distributionpatterns of [11C]PBB3 binding reflect the differences in taudistribution in PSP, CBS and AD patients, which are highlycompatible with neurological manifestation in each disorder.第18回国際パーキンソン病・運動障害疾患会議（MDS2014