Correlations of 18F-THK5351 PET with postmortem burden of tau and astrogliosis in Alzheimer disease

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

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

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-b, 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-b. 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.

Original languageEnglish
Pages (from-to)671-674
Number of pages4
JournalJournal of Nuclear Medicine
Volume59
Issue number4
DOIs
Publication statusPublished - 2018 Apr 1

Keywords

  • Alzheimer’s disease
  • Imaging-pathology correlation
  • PET
  • Tau

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

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