@article{oai:repo.qst.go.jp:00047205,
 author = {Maruyama, Masahiro and Shimada, Hitoshi and Suhara, Tetsuya and Shinotoh, Hitoshi and Ji, Bin and Maeda, Jun and Zhang, Ming-Rong and Q, Trojanowski John and M-Y, Lee Virginia and Ono, Maiko and Masamoto, Kazuto and Takano, Harumasa and Sahara, Naruhiko and Iwata, Nobuhisa and Okamura, Nobuyuki and Furumoto, Shozo and Kudo, Yukitsuka and Chang, Qing and C, Saido Takaomi and Takashima, Akihiko and Lewis, Jada and Jang, Ming-Kuei and Aoki, Ichio and Ito, Hiroshi and Higuchi, Makoto and 丸山 将浩 and 島田 斉 and 須原 哲也 and 篠遠 仁 and 季 斌 and 前田 純 and 張 明栄 and 小野 麻衣子 and 正本 和人 and 高野 晴成 and 佐原 成彦 and 古本 祥三 and 青木 伊知男 and 伊藤 浩 and 樋口 真人},
 issue = {6},
 journal = {Neuron},
 month = {Sep},
 note = {Accumulation of intracellular tau fibrils has been the focus of research on the mechanisms of neurodegeneration in Alzheimer's disease (AD) and related tauopathies. Here, we have developed a class of tau ligands, phenyl/pyridinyl-butadienyl-benzothiazoles/benzothiazoliums (PBBs), for visualizing diverse tau inclusions in brains of living patients with AD or non-AD tauopathies and animal models of these disorders. In vivo optical and positron emission tomographic (PET) imaging of a transgenic mouse model demonstrated sensitive detection of tau inclusions by PBBs. A pyridinated PBB, [(11)C]PBB3, was next applied in a clinical PET study, and its robust signal in the AD hippocampus wherein tau pathology is enriched contrasted strikingly with that of a senile plaque radioligand, [(11)C]Pittsburgh Compound-B ([(11)C]PIB). [(11)C]PBB3-PET data were also consistent with the spreading of tau pathology with AD progression. Furthermore, increased [(11)C]PBB3 signals were found in a corticobasal syndrome patient negative for [(11)C]PIB-PET.},
 pages = {1094--1108},
 title = {Imaging of tau pathology in a tauopathy mouse model and in Alzheimer patients compared to normal controls.},
 volume = {79},
 year = {2013}
}