Abstract
Objective: To investigate the characteristics of tau deposition and its impact on functional connectivity (FC) in Alzheimer’s disease (AD).Methods: Hybrid PET/MRI scans with [18F]-THK5317 and neuropsychological assessments were undertaken in 26 participants with AD and 19 healthy controls (HC). The standardized uptake value ratio (SUVR) of [18F]-THK5317 PET imaging was compared between the AD and HC groups. Significant clusters that revealed higher tau deposition in the AD group compared to the HC group were selected as regions of interest (ROI) for FC analysis. We evaluated the difference in the FC between the two groups for each ROI pair. The clinical and radiological characteristics were compared between the AD patients with negative FC and AD patients with positive FC for exploratory analysis.Results: The bilateral inferior lateral temporal lobe, dorsal prefrontal cortex, precuneus, posterior cingulate cortex, hippocampus, and occipital lobe showed significantly higher [18F]-THK5317 accumulation in AD patients. Decreased FC in regions with higher SUVR was observed in AD patients, and the FC strength was negatively correlated with regional SUVR. Patients with a positive FC exhibited older ages, better cognitive performances, and a lower SUVR than patients with a negative FC.Conclusions: An impact of tau deposition was observed on FC at the individual level in AD patients. Our findings suggested that the combination of tau-PET and rs-fMRI might help predict AD progression.
Highlights
Abnormal deposition of amyloid-β (Aβ) and tau is the hallmark of pathology in Alzheimer’s disease (AD)
In this study, using hybrid positron emission tomography (PET)/MRI with [18F]THK5317, we investigated the characteristics of tau deposition and its impact on functional connectivity (FC) in AD patients at the individual level
The results of the voxel-based morphometry (VBM) analysis of the standardized uptake value ratio (SUVR) maps are shown in Table 2 and Figure 1
Summary
Abnormal deposition of amyloid-β (Aβ) and tau is the hallmark of pathology in Alzheimer’s disease (AD). Tau protein plays an important role in promoting the stability of tubulin assemblies and maintaining the microarchitecture of neurons (Kametani and Hasegawa, 2018). Recent advances in molecular neuroimaging, including positron emission tomography (PET), have enabled the identification and quantification of pathological proteins in vivo. PET with tracers, including [18F]-THK5317 and [18F]-AV1451, is a wellestablished neuroimaging technique for measuring regional tau burden. Previous studies with tau-PET demonstrated that the spatial pattern of tau deposition was similar to the key features of the Braak histopathological stages illustrated by autopsy-based assessments (Schwarz et al, 2016). Compared with Aβ, the spread of tau pathology shows a strong relationship with the progression of AD (Kametani and Hasegawa, 2018)
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