RT Journal Article SR Electronic T1 Correlations of 18F-THK5351 PET with Postmortem Burden of Tau and Astrogliosis in Alzheimer Disease JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 671 OP 674 DO 10.2967/jnumed.117.197426 VO 59 IS 4 A1 Ryuichi Harada A1 Aiko Ishiki A1 Hideaki Kai A1 Naomi Sato A1 Katsutoshi Furukawa A1 Shozo Furumoto A1 Tetsuro Tago A1 Naoki Tomita A1 Shoichi Watanuki A1 Kotaro Hiraoka A1 Yoichi Ishikawa A1 Yoshihito Funaki A1 Tadaho Nakamura A1 Takeo Yoshikawa A1 Ren Iwata A1 Manabu Tashiro A1 Hironobu Sasano A1 Tetsuyuki Kitamoto A1 Kazuhiko Yanai A1 Hiroyuki Arai A1 Yukitsuka Kudo A1 Nobuyuki Okamura YR 2018 UL http://jnm.snmjournals.org/content/59/4/671.abstract 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.