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 Harada, Ryuichi A1 Ishiki, Aiko A1 Kai, Hideaki A1 Sato, Naomi A1 Furukawa, Katsutoshi A1 Furumoto, Shozo A1 Tago, Tetsuro A1 Tomita, Naoki A1 Watanuki, Shoichi A1 Hiraoka, Kotaro A1 Ishikawa, Yoichi A1 Funaki, Yoshihito A1 Nakamura, Tadaho A1 Yoshikawa, Takeo A1 Iwata, Ren A1 Tashiro, Manabu A1 Sasano, Hironobu A1 Kitamoto, Tetsuyuki A1 Yanai, Kazuhiko A1 Arai, Hiroyuki A1 Kudo, Yukitsuka A1 Okamura, Nobuyuki 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.