Objectives:[11C]PBB3 is a novel tau imaging PET ligand, showing high affinity and selectivity for tau deposits. The aim of the present study was to investigate characteristics of [11C]PBB3 binding and its relation with clinical aspects in cognitively healthy subjects and patients with cognitive impairments.Methods:Participants included 17 AD patients, 15 mild cognitive impairments (MCI) patients and 17 age and gender matched cognitively healthy controls (HCs). The PET study was approved by the institutional review board. Written informed consent was obtained from all subjects. PET scans with [11C]PBB3 and an amyloid radioligand, [11C]PIB, and T1-weighted MRI were performed for each individual. Standardized uptake value ratio (SUVR) was calculated for PET images using the cerebellar cortex as reference region. Tau and amyloid deposits were visually assessed using SUVR images for [11C]PBB3 and [11C]PIB, respectively. Correlation between clinical dementia rating scale (CDR) sum of boxes and mean cortical [11C]PBB3 or [11C]PIB SUVR was analyzed among [11C]PIB-positive MCI and AD patients.Results:All HCs and 6 MCI patients were [11C]PIB-negative, and all AD patients and 9 of 15 MCI patients were [11C]PIB-positive. [11C]PBB3 was highly accumulated in the medial temporal cortex of all AD and [11C]PIB-positive MCI patients, in contrast to the modest binding of [11C]PIB in the corresponding region. Distribution of [11C]PBB3 accumulation observed in [11C]PIB-positive MCI patients was restricted within the temporal cortex, while AD patients showed [11C]PBB3 accumulation extending to the neocortex. Some HCs showed accumulation of [11C] PBB3 in the temporal cortex, despite no increase in cortical [11C]PIB binding. Dementia severity (CDR sum of boxes) among AD and [11C]PIB-positive MCI patients showed significant positive correlation with mean cortical [11C]PBB3 binding, but no association with [11C]PIB binding measures..Conclusions:Distribution of [11C]PBB3 binding observed in AD and [11C]PIB-positive MCI patients extended from the temporal area to the entire limbic system and subsequently to the neocortex as a function of disease severity. Some HCs showed noticeable [11C]PBB3 binding in the limbic system, implying that tau deposition may be initiated in a manner independent of amyloid accumulation.第55回日本神経学会学術大
