TY - JOUR
T1 - Correlations of 18F-THK5351 PET with postmortem burden of tau and astrogliosis in Alzheimer disease
AU - Harada, Ryuichi
AU - Ishiki, Aiko
AU - Kai, Hideaki
AU - Sato, Naomi
AU - Furukawa, Katsutoshi
AU - Furumoto, Shozo
AU - Tago, Tetsuro
AU - Tomita, Naoki
AU - Watanuki, Shoichi
AU - Hiraoka, Kotaro
AU - Ishikawa, Yoichi
AU - Funaki, Yoshihito
AU - Nakamura, Tadaho
AU - Yoshikawa, Takeo
AU - Iwata, Ren
AU - Tashiro, Manabu
AU - Sasano, Hironobu
AU - Kitamoto, Tetsuyuki
AU - Yanai, Kazuhiko
AU - Arai, Hiroyuki
AU - Kudo, Yukitsuka
AU - Okamura, Nobuyuki
N1 - Funding Information:
This study was supported by research funds from GE Healthcare; the SEI (Sumitomo Electric Industries, Ltd.) Group CSR Foundation; Health and Labor Sciences Research Grants from the Ministry of Health, Labor, and Welfare of Japan; Grant-in-Aid for Scientific Research (B) (15H04900); Grant-in-Aid for Young Scientists (B) (15K19767); Grant-in-Aid for Scientific Research (B) (25293259); Grant-in-Aid for Scientific Research on Innovative Areas (Brain Protein Aging and Dementia Control) (26117003) from MEXT; and the Japan Research Foundation for Clinical Pharmacology. No other potential conflict of interest relevant to this article was reported.
Publisher Copyright:
� Copyright 2018 SNMMI; all rights reserved.
PY - 2018/4/1
Y1 - 2018/4/1
N2 - 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.
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-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.
KW - Alzheimer’s disease
KW - Imaging-pathology correlation
KW - PET
KW - Tau
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U2 - 10.2967/jnumed.117.197426
DO - 10.2967/jnumed.117.197426
M3 - Article
C2 - 28864633
AN - SCOPUS:85042857620
VL - 59
SP - 671
EP - 674
JO - Journal of Nuclear Medicine
JF - Journal of Nuclear Medicine
SN - 0161-5505
IS - 4
ER -