Objective: Early detection of the brain tau deposition in patients with progressive supranuclear palsy-parkinsonism (PSP-P) by ¹⁸F-PMPBB3 positron emission tomography (PET) imaging.

Background: PSP is a clinical syndrome pathologically characterized by predominant 4-repeat tau aggregation in the brain. Autopsy-confirmed PSP patients have variant clinical presentations. Parkinsonism resembling Parkinson’s disease (PSP-P) is one of these subtypes. The predominant features of PSP-P include bradykinesia and rigidity, response to levodopa, asymmetric onset, and tremor. These PD-mimic presentations cause the low diagnostic accuracy of PD, PSP-P and other subtypes of PSP in the early stage of disease. To develop diagnostic biomarkers for the early diagnosis of PSP-P is critical.

PET studies with a new second-generation of tau ligand, ¹⁸F-PM-PBB3, revealed increased tau deposition in Alzheimer’s disease (AD) and PSP-Richarson syndrome (PSP-RS). To date, there is no report of the ¹⁸F-PM-PBB3 PET imaging in PSP-P patients. Here, we showed the ¹⁸F-PM-PBB3 PET imaging of a patient with PSP-P, a patient with PSP-RS, and a patient with PSP-progressive gait freezing (PSP-PGF).

Method: Subjects received one i.v. administrations of approximately 5mCi (185MBq) ¹⁸F-PMPBB3. PET imaging was performed and analyze by standard methods.

Results: A 56-year-old female had 4-year history of the left leg clumsiness without other atypical signs. The response of levodopa treatment was good in the first three years then gradually declined later. The PET imaging showed the uptake ¹⁸F-PM-PBB3 moderately increased at bilateral globus pallidus (GP), but only slightly increased at the midbrain (Fig 1A). The initial presentations of a 60-year-old patient with PSP-PGF were freezing of gait and frequent fall (forward) for three years. There was no gaze palsy. The ¹⁸F-PM-PBB3 PET imaging showed moderate tau deposition at bilateral GP, as well as the midbrain (Fig 1B). A 63-year-old female PSP-RS patient presented with frequent fall and posture instability in the past four years and followed by vertical gaze palsy. Imaging showed obviously increased ¹⁸F-PM-PBB3 binding at bilateral GP, striatum, brain stem, and the cerebellum (Fig 1C).

Conclusion: The ¹⁸F-PM-PBB3 PET imaging might represent the different tau deposition pattern of the subtypes of PSP. It might be a promising tool to detect the tau burden in vivo in the early stage of non-AD tauopathies.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/tau-pet-imaging-in-a-patient-with-progressive-supranuclear-palsy-parkinsonism-a-case-report/