[11C]PBB3 PET detects tau pathology in corticobasal syndrome and progressive supranuclear palsy.

Objective:[11C]PBB3 has been recently introduced as a tau imaging PET ligand that has high affinity and selectivity for tau deposits. The aim of the present study is to investigate distribution of tau-pathology in progressive supranuclar palsy (PSP) and corticobasal degeneration (CBD) by [11C]PBB3 PET. Methods:Twelve patients with PSP, 8 patients with corticobasal syndrome (CBS), and 25 age-matched healthy controls (HCs) participated in this study. Seventeen patients with Alzheimer’s disease (AD) also took part in as disease control. Sequential PET scans were performed for 70 min following intravenous injection of [11C]PBB3. Standardized uptake value ratio (SUVR) at 30-50 min was calculated using the cerebellar cortex as reference region. Cerebral beta-amyloid depositions were estimated using [11C]Pittsburgh compound B PET. Results:All patients and HCs were PIB-negative except one patient with CBS and 4 HCs. SPM analysis showed high [11C]PBB3 binding in globus pallidus, putamen, thalamus, midbrain, pons, and peri-rolandic areas in PSP patients compared with 21 HCs. Seven PIB-negative CBS patients showed high [11C]PBB3 binding in peri-rolandic areas, supplementary motor area, and midbrain compared with 21 HCs. One PIB-positive patient with CBS showed high [11C]PBB3 binding in the whole cerebral cortex including limbic cortex like AD patients. Conclusion:The distribution of [11C]PBB3 binding in the patients was mostly in agreement with the known distribution of tau pathology in PSP and CBD, suggesting that [11C]PBB3-PET may be useful for the diagnosis of these disorders and therapeutic monitoring of anti-tau therapy.12th International conference on Alzheimer’s disease and Parkinson’s disease and related neurological disorder