18F-FDG, 18F-FP-CIT, and 18F-Florzolotau PET Imaging in Progressive Supranuclear Palsy

PURPOSE: Imaging protocols for progressive supranuclear palsy (PSP) are increasingly incorporating different PET modalities-including 18 F-fluorodeoxyglucose ( 18 F-FDG; cerebral glucose metabolism), 18 F-FP-CIT (dopamine transporter DAT activity), and 18 F-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 18 F-FDG, 18 F-FP-CIT, and 18 F-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, 18 F-FDG PET revealed significant glucose hypometabolism in frontal, parietal, cerebellar, and subcortical regions. 18 F-FP-CIT PET demonstrated reduced DAT availability in the striatum and midbrain. Finally, 18 F-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.