@misc{oai:repo.qst.go.jp:00071630,
 author = {Shimada, Hitoshi and Hirano, Shigeki and Shinotoh, Hitoshi and Furukawa, Shogo and Eguchi, Yoko and Takahata, Keisuke and Kimura, Yasuyuki and Ikoma, Youko and Yamada, Makiko and Zhang, Ming-Rong and Ito, Hiroshi and Higuchi, Makoto and Kuwabara, Satoshi and Suhara, Tetsuya and 島田 斉 and 平野 成樹 and 篠遠 仁 and 古川 彰吾 and 江口 洋子 and 高畑 圭輔 and 木村 泰之 and 生駒 洋子 and 山田 真希子 and 張 明栄 and 伊藤 浩 and 樋口 真人 and 須原 哲也},
 month = {Jun},
 note = {Objective: To investigate characteristics of [11C]PBB3 binding and
its relation with clinical aspects in patients with progressive
supranuclear palsy (PSP) and corticobasal syndrome (CBS).
Background: [11C]PBB3 is a novel tau imaging positron emission
tomography (PET) ligand, which could visualize the tau deposition in
Alzheimer’s disease (AD) and non-AD tauopathies such as PSP,
CBS and frontotemporal dementia.
Methods: Participants included 10 PSP patients, 9 patients with
corticobasal syndrome (CBS), 19 AD patients, and 20 age and
gender matched healthy controls (HCs). A dose (about 10 mCi) of
[11C]PBB3 was intravenously injected and sequential PET scans
were performed for 70 min. We also performed PET scan with a
plaque-binding agent, [11C]PIB (about 10 mCi), for 70 min and threedimensional
T1-weighted MRI. Standardized uptake value ratio
(SUVR) was calculated for each PET image using the cerebellar
cortex as reference region. Amyloid deposition was verified by visual
assessment of SUVR images of [11C]PIB PET. As for [11C]PBB3
PET data, group analysis among each group was performed by oneway
ANOVA 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 PIBpositive
CBS and two PIB-negative AD patients were excluded from
group analysis. [11C]PBB3 was accumulated in lesions associated
with neurological symptoms in PSP, CBS and AD patients. To be
specific, [11C]PBB3 binding was significantly increased in the
brainstem, basal ganglia, thalamus and dentate nucleus in PSP
patients compared to HCs. In PIB-negative CBS patients,
remarkable uptake of [11C]PBB3 was observed in basal ganglia and
the neocortex including the supplementary motor area (SMA) and
the peri-Rolandic area compared to HCs. Furthermore, [11C]PBB3
retention observed in PIB-positive CBS patient extended the
neocortex as well as the entire limbic system, resembling AD
patients with profound cognitive decline. Some brain lesions with
[11C]PBB3 binding exhibited brain atrophy in PSP, CBS and AD
patients.
Conclusions: The present study demonstrated that distribution
patterns of [11C]PBB3 binding reflect the differences in tau
distribution in PSP, CBS and AD patients, which are highly
compatible 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）},
 title = {In vivo tau PET imaging using [11C]PBB3 in patients with PSP and CBS},
 year = {2014}
}