PT - JOURNAL ARTICLE AU - Ryuichi Harada AU - Aiko Ishiki AU - Hideaki Kai AU - Naomi Sato AU - Katsutoshi Furukawa AU - Shozo Furumoto AU - Tetsuro Tago AU - Naoki Tomita AU - Shoichi Watanuki AU - Kotaro Hiraoka AU - Yoichi Ishikawa AU - Yoshihito Funaki AU - Tadaho Nakamura AU - Takeo Yoshikawa AU - Ren Iwata AU - Manabu Tashiro AU - Hironobu Sasano AU - Tetsuyuki Kitamoto AU - Kazuhiko Yanai AU - Hiroyuki Arai AU - Yukitsuka Kudo AU - Nobuyuki Okamura TI - Correlations of <sup>18</sup>F-THK5351 PET with Postmortem Burden of Tau and Astrogliosis in Alzheimer Disease AID - 10.2967/jnumed.117.197426 DP - 2018 Apr 01 TA - Journal of Nuclear Medicine PG - 671--674 VI - 59 IP - 4 4099 - http://jnm.snmjournals.org/content/59/4/671.short 4100 - http://jnm.snmjournals.org/content/59/4/671.full SO - J Nucl Med2018 Apr 01; 59 AB - Clinical PET studies using 18F-THK5351 have demonstrated significant tracer retention in sites susceptible to tau burden in Alzheimer disease (AD). However, the in vivo PET signal to reflect tau aggregates remains controversial. Methods: We examined the spatial pattern of tracer binding, amyloid-β, tau, and gliosis in an autopsy-confirmed AD patient who underwent 18F-THK5351 and 11C-Pittsburgh compound B PET before death. Results: Regional in vivo 18F-THK5351 retention was significantly correlated with the density of tau aggregates in the neocortex and monoamine oxidase-B in the whole brain, but not correlated with that of insoluble amyloid-β. Furthermore, significant association was observed between the density of tau aggregates, monoamine oxidase-B, and glial fibrillary acidic protein, suggesting that neocortical tau would strongly influence the formation of reactive astrocytes. Conclusion: 18F-THK5351 PET may have limited utility as a biomarker of tau pathology in AD; however, it could be used to monitor the neuroinflammatory processes in the living brain.