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PET imaging of tau pathology in progressive supranuclear palsy

S. Coakeley, S.S. Cho, P. Rusjan, A. Graff-Guerrero, R. Chen, A.E. Lang, L. Kalia, E. Slow, S. Houle, A.P. Strafella (Toronto, ON, Canada)

Meeting: 2016 International Congress

Abstract Number: 1164

Keywords: Positron emission tomography(PET), Progressive supranuclear palsy(PSP), Tauopathies

Session Information

Date: Wednesday, June 22, 2016

Session Title: Neuroimaging (non-PD)

Session Time: 12:00pm-1:30pm

Location: Exhibit Hall located in Hall B, Level 2

Objective: This study aimed to determine whether there is an increase in [18F]-AV-1451 uptake in the brains of progressive supranuclear palsy (PSP) patients compared to Parkinson’s disease (PD) patients and healthy controls (HC).

Background: PSP is a rare form of parkinsonism that differs neuropathologically from other Parkinsonian disorders; however, there is often an overlap of clinical symptoms, especially in the early stages of PSP. While PD, Lewy body dementia, and multiple system atrophy are classified as synucleinopathies, PSP is a tauopathy due to the aggregation of pathological tau in the brain. [18F]-AV-1451 (also known as [18F]-T807) is a positron emission tomography (PET) radiotracer that binds to paired helical filaments (PHF) of tau in Alzheimer’s disease (AD), as shown previously in clinical studies. We investigated whether [18F]-AV-1451 could be used as biomarker for the diagnosis and disease progression monitoring in PSP.

Methods: A total of 11 patients (5 PSP: age 74.0±5.65, 3 female; and 6 PD: age 63.7±9.61, 3 female) and 8 age-matched HC (age 63.3±9.11, 8 female) were recruited. An anatomical MRI and a 90-minute PET scan, using [18F]-AV-1451, were acquired from all participants. The standardized uptake value ratio (SUVR) from 30 to 60 minutes post-injection was calculated in each region of interest (ROI) with the cerebellum, as well as the corpus callosum as reference regions. ROIs were selected based on cortical and subcortical brain regions previously reported to present with tau pathology in PSP. A nonparametric Kruskal–Wallis test was employed to check for differences in SUVR between the three groups.

Results: Differences in age and gender across groups were not significant. There were no significant increases of [18F]-AV-1451 SUVR in PSP compared to PD and HC in any of the tested cortical and subcortical ROIs. These results were reliable when analyzed using the two different reference regions (i.e. cerebellum and corpus callosum).

Conclusions: No differences in SUVR could be detected in any of our PSP patients compared to controls. Any uptake in tracer could have been potential off target binding. Our preliminary results suggest that using SUVR on [18F]-AV-1451 images may not be an appropriate marker for abnormal tau deposition in PSP.

To cite this abstract in AMA style:

S. Coakeley, S.S. Cho, P. Rusjan, A. Graff-Guerrero, R. Chen, A.E. Lang, L. Kalia, E. Slow, S. Houle, A.P. Strafella. PET imaging of tau pathology in progressive supranuclear palsy [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/pet-imaging-of-tau-pathology-in-progressive-supranuclear-palsy/. Accessed June 14, 2025.
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