Abstract
Background: Tau pathology is an important component of Alzheimer’s Disease but its extent and impact in cognitively healthy patients with cerebral amyloid angiopathy (CAA) are not clear. We compared in vivo tau stages estimated from the patterns of tau PET tracer uptake in patients with CAA and healthy controls (HC) and explored its relationship with amyloid burden and cognitive function in CAA. Methods: The study included 50 cognitively healthy probable CAA patients (mean age 70±7.6) and 50 age-, sex-matched HCs (mean age 70±7.5) who underwent MRI, Pittsburgh compound B (PiB, for amyloid) and 18 F-flortaucipir (FTP, for tau) PET imaging. Mean global cortical PiB uptake was calculated. Tau stages were estimated based on the distribution pattern of cortical FTP uptake and grouped into three categories (PET Braak Staging, Figure). Within the CAA cohort, standardized z-scores of memory, processing speed and executive function testing were obtained. Results: In the whole group, tau stages significantly correlated with age (rho=0.407, p<0.001) and global cortical PiB uptake (rho=0.554, p<0.001). Patients with CAA were more likely to exhibit more extensive tau (Stage III-VI) compared to HCs in univariate analyses (Figure, p=0.003). In a logistic regression model, more extensive tau independently associated with age (p=0.001) and PiB uptake (p<0.001) but not with the CAA diagnosis (p=0.264). Within the CAA cohort, tau stage was again independently associated with PiB uptake (p=0.002), but it did not show any association with scores of cognitive domains in univariate or multivariate models (p>0.2 for all comparisons). Conclusion: Our results show that patients with CAA have higher PET Braak tau stages when compared to similarly aged HCs but this difference disappeared after controlling for amyloid load. Extent of tau did not correlate with cognitive scores in CAA. Overall, tau stages appear to be driven by amyloid without clinical impact in cognitively healthy CAA patients.
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