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Abstract #2654

Hyperperfusion in middle-aged individuals with genetic risk of sporadic Alzheimer’s disease

Maria-Eleni Dounavi1, Elijah Mak1, Audrey Low1, Guy B Williams2, Katie Wells3, Graciela Muniz-Terrera3,4, Brian Lawlor5, Lorina Naci5, Paresh Malhotra6, Ivan Koychev7, Karen Ritchie8, Li Su1,9, Craig W Ritchie3, and John T O'Brien1
1Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom, 2Department of Clinical Neurosciences and Wolfson Brain Imaging Centre, University of Cambridge, Cambridge, United Kingdom, 3Centre for Dementia Prevention, University of Edinburgh, Edinburgh, United Kingdom, 4Ohio University, Athens, OH, United States, 5Institute of Neuroscience, Trinity College Dublin, University of Dublin, Dublin, United Kingdom, 6Division of Brain Science, Imperial College Healthcare NHS Trust, London, United Kingdom, 7Department of Psychiatry, University of Oxford, Oxford, United Kingdom, 8INSERM, Montpellier, France, 9University of Sheffield, Sheffield, United Kingdom

Synopsis

Keywords: Alzheimer's Disease, Arterial spin labellingExtensive brain hypoperfusion is well-established in people with Alzheimer’s disease (AD). However, mixed findings have emerged during the pre-symptomatic disease stage. In this study, we used arterial spin labelling (ASL) MRI in middle-aged, cognitively normal participants from the PREVENT-Dementia study to evaluate cerebral perfusion differences between carriers and non-carriers of the apolipoprotein ε4 (APOE4) allele. The ASL spatial coefficient of variation (CoV) was used as a proxy for arterial transit time (ATT) delays. We found hyperperfusion in APOE4 carriers which was not accompanied by increased spatial CoV, suggesting that the observed hyperperfusion is not driven by ATT delays.

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