18F-FDG, 18F-FP-CIT, and 18F-Florzolotau PET Imaging in Progressive Supranuclear Palsy: Region-Specific Correlations Between Glucose Metabolism, Dopaminergic Function, and Tau Pathology
- PMID: 41474764
- DOI: 10.1097/RLU.0000000000006254
18F-FDG, 18F-FP-CIT, and 18F-Florzolotau PET Imaging in Progressive Supranuclear Palsy: Region-Specific Correlations Between Glucose Metabolism, Dopaminergic Function, and Tau Pathology
Abstract
Purpose: Imaging protocols for progressive supranuclear palsy (PSP) are increasingly incorporating different PET modalities-including 18F-fluorodeoxyglucose (18F-FDG; cerebral glucose metabolism), 18F-FP-CIT (dopamine transporter [DAT] activity), and 18F-Florzolotau (tau pathology) PET-to improve diagnostic accuracy. In this cross-sectional study, we characterized tracer-specific imaging patterns and evaluated their interrelationships in patients with PSP to clarify the underlying pathophysiological mechanisms.
Materials and methods: Twenty-eight patients with clinically diagnosed PSP underwent 18F-FDG, 18F-FP-CIT, and 18F-Florzolotau PET imaging. Quantitative voxel-based and region-of-interest analyses were conducted. Standardized uptake value ratios (SUVRs) were calculated and compared with sex-matched controls (n=20 per PET modality).
Results: In patients with PSP compared with controls, 18F-FDG PET revealed significant glucose hypometabolism in frontal, parietal, cerebellar, and subcortical regions. 18F-FP-CIT PET demonstrated reduced DAT availability in the striatum and midbrain. Finally, 18F-Florzolotau PET showed elevated tau deposition in the thalamus, midbrain, pons, and precentral gyrus. An inverse correlation linked midbrain tau burden with local glucose metabolism (r=-0.39, P=0.04). Frontal hypometabolism correlated strongly with subcortical metabolic deficits (r=0.61, P<0.001). Only the left putamen showed a moderate negative association between DAT loss and tau accumulation (r=-0.42, P=0.03).
Conclusions: Patients with PSP exhibit metabolic deficits in cortical-subcortical networks, dopaminergic denervation in striatal-midbrain regions, and tau pathology localized to brainstem and thalamic areas. Tracer-specific SUVRs correlations revealed specific interplay among glucose hypometabolism, DAT deficiency, and tau accumulation.
Keywords: cerebral glucose metabolism; dopamine transporter; positron emission tomography; progressive supranuclear palsy; tau pathology.
Copyright © 2025 Wolters Kluwer Health, Inc. All rights reserved.
Conflict of interest statement
Conflicts of interest and sources of funding: This study was supported by the National High-Level Hospital Clinical Research Funding (grant number 2025-PUMCH-D-003), the National Natural Science Foundation of China (grant number 82402335 and 12205329), and Ye Ming Han Fund (2024) (grant number X21520603). T.-C.Y. is an employee and shareholder of APRINOIA Therapeutics Co., Ltd. (Suzhou, China). All other authors report no relevant financial or non-financial conflicts of interest.
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