Abstract
Background and Objective: Tau-specific positron emission topography (PET) imaging enables in vivo assessment of Alzheimer's disease (AD). We aimed to investigate its performance in combination with plasma tau levels in patients with non-AD tauopathy.Methods: A total of 47 participants were enrolled, including 10 healthy controls, 16 with tauopathy parkinsonism syndromes (9 with corticobasal syndrome [CBS], 7 with progressive supranuclear palsy [PSP]), 9 with frontotemporal dementia (FTD), 4 with AD, and 8 with Parkinson's disease (PD). All participants underwent clinical assessments, 18F-T807 tau PET, brain MRI, and plasma tau assay.Results: The global cortical standard uptake value ratio (SUVR) of 18F-T807 PET was comparable between PD and control (p = 0.088). The cortical SUVR was significantly higher in AD group (p = 0.002) but was modestly increased in PSP group compared to the PD group (p = 0.044), especially in parietal and pallidal regions. Asymmetric 18F-T807 uptake at the pallidum was noted in patients with CBS and FTD. Cortical tau tracer uptake was associated with increased plasma total tau level (p = 0.016), especially in frontal and parietal regions. Regional tracer uptake was correlated with cortical thinning in patients with CBS and PSP (CBS: r = −0.092, p = 0.025; PSP: r = −0.114, p = 0.015).Conclusions: The 18F-T807 tau tracer uptake was only modestly increased in patients with PSP. Although the cortical tau tracer uptake correlated with regional cortical atrophy and plasma tau levels, a four-repeated tau-specific tracer is needed for future classifying tauopathy parkinsonism syndromes.
Highlights
Misfolded tau protein deposits in neurons represent the neuropathological hallmark in many neurodegenerative disorders, including Alzheimer’s disease (AD), frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), argyrophilic grain disease, and Down syndrome (Murray et al, 2014; Wang and Edison, 2019)
Tau is encoded by the microtubule-associated protein tau (MAPT) gene, and alternative splicing results in six tau isoforms in human brain, categorized into three-repeat (3R) or four-repeat (4R) tau according to the number of carboxy-terminal repeat domains (Wang and Mandelkow, 2015)
Of all the tau positron emission tomography (PET) tracers, 18F-T807 is the most widely applied in patients with neurodegenerative diseases and has been the first tau PET tracer approved by the U.S Food and Drug Administration (Okamura et al, 2014a; Barthel, 2020; Fleisher et al, 2020)
Summary
Misfolded tau protein deposits in neurons represent the neuropathological hallmark in many neurodegenerative disorders, including Alzheimer’s disease (AD), frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), argyrophilic grain disease, and Down syndrome (Murray et al, 2014; Wang and Edison, 2019). The advent of tau-specific positron emission tomography (PET) has enabled in vivo detection of pathological tau aggregates in patients with AD (Ossenkoppele et al, 2016; Mattsson et al, 2017). An alternative approach to assess tau pathology in vivo is measurement of biofluid levels of tau. Plasma levels of phosphorylated tau (p-tau181) were recently shown to be a surrogate blood-based biomarker of AD (Karikari et al, 2020). Studies examining the applications of either tau PET imaging or blood-based tau biomarkers in assisting the diagnosis of non-AD tauopathies are still few. Tau-specific positron emission topography (PET) imaging enables in vivo assessment of Alzheimer’s disease (AD). We aimed to investigate its performance in combination with plasma tau levels in patients with non-AD tauopathy
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