Correlations of ¹⁸F-THK5351 PET with Postmortem Burden of Tau and Astrogliosis in Alzheimer Disease

This is the authors' abstract. We don't add key points for this paper.

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.