Suboptimal self‐reported sleep efficiency and duration are associated with faster accumulation of brain amyloid beta in cognitively unimpaired older adults
Louise N Pivac, B. Brown, Kelsey R. Sewell, J. Doecke, V. Villemagne, V. Doré, M. Weinborn, H. Sohrabi, S. Gardener, R. Bucks, Simon M. Laws, K. Taddei, P. Maruff, Colin L. Masters, Christopher C. Rowe, Ralph N. Martins, S. Rainey-Smith
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Abstract
Abstract INTRODUCTION This study investigated whether self‐reported sleep quality is associated with brain amyloid beta (Aβ) accumulation. METHODS Linear mixed effect model analyses were conducted for 189 cognitively unimpaired (CU) older adults (mean ± standard deviation 74.0 ± 6.2; 53.2% female), with baseline self‐reported sleep data, and positron emission tomography‐determined brain Aβ measured over a minimum of three time points (range 33.3–72.7 months). Analyses included random slopes and intercepts, interaction for apolipoprotein E (APOE) ε4 allele status, and time, adjusting for sex and baseline age. RESULTS Sleep duration <6 hours, in APOE ε4 carriers, and sleep efficiency <65%, in the whole sample and APOE ε4 non‐carriers, is associated with faster accumulation of brain Aβ. DISCUSSION These findings suggest a role for self‐reported suboptimal sleep efficiency and duration in the accumulation of Alzheimer's disease (AD) neuropathology in CU individuals. Additionally, poor sleep efficiency represents a potential route via which individuals at lower genetic risk may progress to preclinical AD. Highlights In cognitively unimpaired older adults self‐report sleep is associated with brain amyloid beta (Aβ) accumulation. Across sleep characteristics, this relationship differs by apolipoprotein E (APOE) genotype. Sleep duration <6 hours is associated with faster brain Aβ accumulation in APOE ε4 carriers. Sleep efficiency < 65% is associated with faster brain Aβ accumulation in APOE ε4 non‐carriers. Personalized sleep interventions should be studied for potential to slow Aβ accumulation.