Screening of [(18)F]Florbetazine for Aβ Plaques and a Head-to-Head Comparison Study with [(11)C]Pittsburgh Compound-B ([(11)C]PiB) in Human Subjects

在人体受试者中对 [(18)F]Florbetazine 进行 Aβ 斑块筛查,并与 [(11)C]Pittsburgh Compound-B ([(11)C]PiB) 进行头对头比较研究

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Abstract

Positron emission tomography (PET) imaging of amyloid-β (Aβ) has emerged as a crucial strategy for early diagnosis and monitoring of therapeutic advancements targeting Aβ. In our previous first-in-human study, we identified that [(18)F]Florbetazine ([(18)F]92), featuring a diaryl-azine scaffold, exhibits higher cortical uptake in Alzheimer's disease (AD) patients compared to healthy controls (HC). Building upon these promising findings, this study aimed to characterize the diagnostic potential of [(18)F]92 and its dimethylamino-modified tracer [(18)F]91 and further compare them with the benchmark [(11)C]PiB in the same cohort of AD patients and age-matched HC subjects. The cortical accumulation of these tracers was evident, with no significant radioactivity retention observed in the cortex of HC subjects, consistent with [(11)C]PiB images (correlation coefficient of 0.9125 and 0.7883 between [(18)F]Florbetazine/[(18)F]91 and [(11)C]PiB, respectively). Additionally, quantified data revealed higher standardized uptake value ratios (SUVR) (with the cerebellum as the reference region) of [(18)F]Florbetazine/[(18)F]91 in AD patients compared to the HC group ([(18)F]Florbetazine: 1.49 vs 1.16; [(18)F]91: 1.33 vs 1.20). Notably, [(18)F]Florbetazine exhibited less nonspecific bindings in myelin-rich regions, compared to the dimethylamino-substituted [(18)F]91, akin to [(11)C]PiB. Overall, this study suggests that [(18)F]Florbetazine displays superior characteristics to [(18)F]91 in identifying Aβ pathology in AD. Furthermore, the close agreement between the uptakes in nontarget regions for [(18)F]Florbetazine and [(11)C]PiB in this head-to-head comparison study underscores its suitability for both clinical and research applications.

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