@misc{oai:repo.qst.go.jp:00071552,
 author = {Suhara, Tetsuya and Shimada, Hitoshi and Shinotoh, Hitoshi and Hirano, Shigeki and Eguchi, Yoko and Takahata, Keisuke and Kimura, Yasuyuki and Yamada, Makiko and Ito, Hiroshi and Higuchi, Makoto and Suhara, Tetsuya and Shimada, Hitoshi and Shinoto, Hitoshi and Hirano, Shigeki and Eguchi, Yoko and Takahata, Keisuke and Kimura, Yasuyuki and Yamada, Makiko and Ito, Hiroshi and Higuchi, Makoto},
 month = {Jun},
 note = {Objectives:
[11C]PBB3 is a novel tau imaging PET ligand, which could visualize the tau deposition in Alzheimer’s disease (AD) and non-AD tauopathies. 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 15 AD patients, 15 mild cognitive impairments (MCI) patients, few patients with corticobasal syndrome (CBS), progressive supranuclear palsy (PSP) and frontotemporal dementia (FTD) and 23 healthy controls (HCs). We performed [11C]PBB3 PET and [11C]PIB PET. Standardized uptake value ratio (SUVR) was calculated for each PET image using the cerebellar cortex as reference region. 
Results:
All HCs and patients with non-AD tauopaties were PIB-negative, and all AD patients and 9 of 15 MCI patients were PIB-positive. [11C]PBB3 was highly accumulated in the medial temporal cortex of all AD and PIB-positive MCI patients, in which binding of [11C]PIB was minimal. Distribution of [11C]PBB3 accumulation observed in AD and PIB-positive MCI patients extended to the entire limbic system and subsequently to the neocortex as a function of the disease severity. Mean cortical [11C]PBB3 binding showed significantly positive correlation with dementia severity among AD and PIB-positive MCI patients. Furthermore, [11C] PBB3 was also accumulated in lesions associated with neurological symptoms in CBS, PSP and FTD patients, as well as some PIB-negative MCI patients and HCs. 
Conclusions:
The present study demonstrated the spread of [11C]PBB3 binding reflect the dementia severity in AD and MCI due to AD patients. Furthermore, [11C]PBB3 binding could explain the neurological manifestations in CBS, PSP and FTD patients.
Research support: “Integrated research on neuropsychiatric disorders”, “J-AMP”, Young Scientists 21791158, Scientific Research (B) 23390235, Core Research for Evolutional Science and Technology and Scientific Research on Innovative Areas 23111009 from the MEXT, Japan, Comprehensive Research on Dementia (No. 11103404) from MHLW, and the Mochida Memorial Foundation for Medical and Pharmaceutical Research., Society of Nuclear Medicine and Molecular Imaging 2014},
 title = {In vivo tau PET imaging using [11C]PBB3 in Alzheimer’s disease and non-Alzheimer’s disease tauopathies.},
 year = {2014}
}