@article{oai:repo.qst.go.jp:00080020,
 author = {Barron, Anna and Ji, Bin and MasayukiFujinaga and Ming-Rong, Zhang and Sahara, Naruhiko and Aoki, Ichio and Tsukada, Hideo and Higuchi, Makoto and Barron, Anna and Ji, Bin and Fujinaga, Masayuki and Ming-Rong, Zhang and Suhara, Tetsuya and Aoki, Ichio and Tsukada, Hideo and Higuchi, Makoto},
 journal = {Neurobiology of Aging},
 month = {May},
 note = {Damaged mitochondria may be one of the earliest manifestations of Alzheimer`s disease (AD). Since oxidative phosphorylation is a primary source of neuronal energy, unlike glycolysis-dependent energy production in inflamed glia, mitochondrial respiration could provide a selective biomarker of neuronal deterioration in AD. Here we used a recently developed positron emission tomography (PET) probe targeting mitochondrial complex I (MC-I), 18F-BCPP-EF, to non-invasively visualize mitochondrial abnormalities in the brains of tau transgenic mice (rTg4510 TauTg). Tauopathy and neuroinflammation were visualized by PET using a tau probe 11C-PBB3 and a TSPO probe, 18F-FEBMP, respectively. A marked reduction in 18F-BCPP-EF uptake was observed in hippocampal and forebrain regions of TauTg mice, colocalizing with regions of tauopathy, neuronal damage and neuroinflammation. MC-I signals were highly correlated with atrophy assayed by MRI, but negatively associated with inflammatory signals measured by TSPO-PET, indicating that neuronal metabolic signals measured by MC-I PET were robust to inflammatory interference. MC-I may be a useful imaging biomarker to detect neuronal damage and metabolic changes with minimal interference from concomitant glial hypermetabolism.},
 pages = {140--148},
 title = {In vivo PET imaging of mitochondrial abnormalities in a mouse model of tauopathy},
 volume = {94},
 year = {2020}
}