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Purpose: Individualised predictive models of cognitive decline require disease-monitoring markers that are repeatable. For wide-spread adoption, such markers also need to be reproducible at different locations. This study assessed the repeatability and reproducibility of MRI markers derived from a dementia protocol., Methods: Six participants were scanned at three different sites with a 3T MRI scanner. The protocol employed: T1-weighted (T1w) imaging, resting state functional MRI (rsfMRI), arterial spin labelling (ASL), diffusion-weighted imaging (DWI), T2-weighted fluid attenuation inversion recovery (FLAIR), T2-weighted (T2w) imaging, and susceptibility weighted imaging (SWI). Participants were scanned repeatedly, up to six times over a maximum period of five years. One participant was also scanned a further three times on sequential days on one scanner. Fifteen derived metrics were computed from the seven different modalities., Results: Reproducibility (coefficient of variation; CoV, across sites) was best for T1w derived grey matter, white matter and hippocampal volume (CoV < 1.5%), compared to rsfMRI and SWI derived metrics (CoV, 19% and 21%). For a given metric, long-term repeatability (CoV across time) was comparable to reproducibility, with short-term repeatability considerably better., Conclusions: Reproducibility and repeatability were assessed for a suite of markers calculated from a dementia MRI protocol. In general, structural markers were less variable than functional MRI markers. Variability over time on the same scanner was comparable to variability measured across different scanners. Overall, the results support the viability of multi-site longitudinal studies for monitoring cognitive decline., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Associazione Italiana di Fisica Medica e Sanitaria. Published by Elsevier Ltd. All rights reserved.)

Cerebral blood flow (CBF) measured with arterial spin labelling (ASL) magnetic resonance imaging (MRI) reflects cerebral perfusion, related to metabolism, and arterial transit time (ATT), related to vascular health. Our aim was to investigate the spatial coefficient of variation (sCoV) of CBF maps as a surrogate for ATT, in volunteers meeting criteria for subjective cognitive decline (SCD), amnestic mild cognitive impairment (MCI) and probable Alzheimer's dementia (AD). Whole-brain pseudo continuous ASL MRI was performed at 3 T in 122 participants (controls = 20, SCD = 44, MCI = 45 and AD = 13) across three sites in New Zealand. From CBF maps that included all grey matter, sCoV progressively increased across each group with increased cognitive deficit. A similar overall trend was found when examining sCoV solely in the temporal lobe. We conclude that sCoV, a simple to compute imaging metric derived from ASL MRI, is sensitive to varying degrees of cognitive changes and supports the view that vascular health contributes to cognitive decline associated with Alzheimer's disease., (© 2021. The Author(s).)

Aotearoa New Zealand's population is ageing. Increasing life expectancy is accompanied by increases in prevalence of Alzheimer's Disease (AD) and ageing-related disorders. The multicentre Dementia Prevention Research Clinic longitudinal study aims to improve understanding of AD and dementia in Aotearoa, in order to develop interventions that delay or prevent progression to dementia. Comprising research clinics in Auckland, Christchurch and Dunedin, this multi-disciplinary study involves community participants who undergo biennial investigations informed by international protocols and best practice: clinical, neuropsychological, neuroimaging, lifestyle evaluations, APOE genotyping, blood collection and processing. A key research objective is to identify a 'biomarker signature' that predicts progression from mild cognitive impairment to AD. Candidate biomarkers include: blood proteins and microRNAs, genetic, neuroimaging and neuropsychological markers, health, cultural, lifestyle, sensory and psychosocial factors. We are examining a range of mechanisms underlying the progression of AD pathology (e.g. faulty blood–brain barrier, excess parenchymal iron, vascular dysregulation). This paper will outline key aspects of the Dementia Prevention Research Clinic's research, provide an overview of data collection, and a summary of 266 participants recruited to date. The national outreach of the clinics is a strength; the heart of the Dementia Prevention Research Clinics are its people. [ABSTRACT FROM AUTHOR]