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| Home > Publications Database > Multicenter [18F]PI-2620 PET for in vivo staging of tau pathology in progressive supranuclear palsy: a subtype/stage inference algorithm study |
| Home > Publications Database > Multicenter [18F]PI-2620 PET for in vivo staging of tau pathology in progressive supranuclear palsy: a subtype/stage inference algorithm study |
| Journal Article | DZNE-2026-00787 |
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2026
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Please use a persistent id in citations: doi:10.1016/j.eanmj.2026.100226
Abstract: Progressive supranuclear palsy (PSP) is a primary 4R tauopathy. Postmortem studies identified six tau pathological stages with tau aggregation with involvement of the subthalamic nucleus and the globus pallidus, with further affliction of the striatum, cerebellum with dentate nucleus, frontal and/or occipital cortices. We aimed to test whether this staging system is also observed when an unsupervised machine learning model is used to analyze in vivo [18F]PI-2620 tau PET imaging data. Furthermore, regional differences in tau tracer binding in different PSP subtypes and corresponding clinical profiles were investigated. Methods: We analyzed imaging and clinical data of 120 patients with the clinical diagnosis of PSP and of 16 healthy controls. Dynamic [18F]PI-2620 PET imaging in a multicenter setting (sites in Germany and Australia) was performed over 60min. After kinetic modeling, parametric distribution volume ratio images were analyzed and classified into different pattern subtypes and stages by use of the SuStaIn algorithm. Regional differences in tau tracer binding were assessed using statistical parametric mapping. Results: The SuStaIn model distinguished three patterns of [18F]PI-2620 binding: i) a subcortical pattern, ii) a rhombencephalic pattern, and iii) a cortical pattern. The subcortical pattern showed a spatiotemporal distribution similar to the previously published PSP postmortem staging system. Subjects in different SuStaIn-derived patterns showed different clinical characteristics, including a significant association with sex (P < 0.001). Conclusion: These results provide motivation to further develop [18F]PI-2620 as an imaging biomarker of PSP. They also demonstrate the potential of the SuStaIn model to reveal so-far-unknown tau tracer binding patterns in PSP, with possible implications for improved phenotyping and future anti-tau treatment decisions.
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