81 Tau PET and cognition INTRODUCTION [18F]Flortaucipir is the most widely studied PET tracer to date for detecting AD-specific tau pathology [1]. Most studies with [18F]flortaucipir used static scan protocols, which allow semi-quantitative estimates such as the standardized uptake value ratio (SUVR) [1]. Advantages of static over dynamic scanning protocols include the relatively short scan duration and computational simplicity which facilitates clinical applicability [2]. On the other hand, dynamic acquisition allows optimal quantitative accuracy and additionally enables computation of parametric images of tracer delivery, which can be interpreted as a proxy of relative tracer flow or relative cerebral blood flow (rCBF) (i.e. R1) [2–9]. R1 represents the ratio between the rate constant for ligand transfer from blood to tissue (K1) in the tissue of interest and the reference region [4–8], which is strongly correlated with metabolic activity derived from [18F]FDG PET [4, 5, 9]. A dynamic [18F]flortaucipir PET scan may thus not only provide accurate information on (regional) quantification of tau pathology, but also yields information on rCBF. Previous studies demonstrated that high levels of regional tau pathology [10–12], as well as low levels of rCBF (as measured with [18F]FDG PET or MRI) [9, 13], correlate with cognitive impairment in various domains. However, rCBF has not been investigated yet using [18F]flortaucipir R 1. Investigating tau pathology and rCBF simultaneously by using dynamic [18F]flortaucipir PET might yield valuable information, since both pathophysiological mechanisms may contribute to cognitive impairment in AD. The aims of this study are to investigate the (regional) association between tau pathology and rCBF, and their (independent) associations with cognitive functioning in patients with AD. METHODS Recruitment of participants Patients were recruited from the Amsterdam Dementia Cohort of the Alzheimer Center Amsterdam [14]. All subjects underwent a standardized dementia screening, including medical and neurological examination, informant-based history, assessment of vital functions, screening laboratory tests, neuropsychological evaluation, MRI, lumbar puncture and/or amyloid-β positron emission tomography (PET), after which diagnoses were determined in a multidisciplinary consensus meeting [14]. For this study, patients with a diagnosis of Alzheimer’s disease (AD) dementia [15] or mild cognitive impairment (MCI) due to AD [16] were included. For all subjects, AD biomarkers in cerebrospinal fluid (CSF) and/or Aβ PET were abnormal (CSF Aβ42 4
RkJQdWJsaXNoZXIy MjY0ODMw