@misc{oai:repo.qst.go.jp:00071878,
 author = {Barron, Anna and Ji, Bin and Fujinaga, Masayuki and Zhang, Ming-Rong and Suhara, Tetsuya and Sahara, Naruhiko and Tsukada, Hideo and Higuchi, Makoto and Ｂａｒｒｏｎ Ａｎｎａ and 季 斌 and 藤永 雅之 and 張 明栄 and 須原 哲也 and 佐原 成彦 and 樋口 真人},
 month = {Oct},
 note = {Damaged mitochondria may be one of the earliest manifestations of Alzheimer`s disease (AD), with region-specific reductions in cerebral metabolism and mitochondrial dysfunction observed long before the onset of symptoms both clinically and in mouse models of the disease. In this study functional imaging was used to examine neuronal metabolic abnormalities in a mouse model of tauopathy (rTg4510) in vivo, using a novel PET probe for mitochondrial complex I (18F-BCPP-EF) which mediates the first step in oxidative phosphorylation. A marked reduction in 18F-BCPP-EF uptake was observed in hippocampal and forebrain regions of rTg4510 mice, coinciding with tau neuropathology as assessed by [11C]PBB3 PET. Further, hippocampal 18F-BCPP-EF uptake positively correlated with hippocampal volume assessed by MRI, indicating an association between mitochondrial complex I and neuronal loss. These findings indicate that mitochondrial complex I may be a useful imaging biomarker for the identification of early-stage metabolic changes associated with AD neuropathology and neuronal loss., 脳タンパク質老化と認知症制御　第１回国際シンポジウム},
 title = {In vivo PET imaging of mitochondrial abnormalities in a mouse model of tauopathy},
 year = {2015}
}