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.
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自我报告的睡眠效率和持续时间不达标与认知能力未受损的老年人大脑淀粉样蛋白 beta 的快速积累有关
摘要 本研究调查了自我报告的睡眠质量是否与大脑淀粉样β(Aβ)的积累有关。方法 对189名认知功能未受损(CU)的老年人(平均值±标准差为74.0±6.2;53.2%为女性)进行线性混合效应模型分析,这些老年人提供了基线自我报告睡眠数据,并在至少三个时间点(范围为33.3-72.7个月)测量了正电子发射断层扫描测定的脑淀粉样β。分析包括随机斜率和截距、载脂蛋白 E (APOE) ε4等位基因状态与时间的交互作用,并对性别和基线年龄进行了调整。结果 在 APOE ε4 携带者中,睡眠持续时间小于 6 小时;在整个样本和 APOE ε4 非携带者中,睡眠效率小于 65%,这与大脑 Aβ 的快速积累有关。讨论 这些研究结果表明,自我报告的睡眠效率和持续时间不达标会导致阿尔茨海默病(AD)神经病理学在 CU 患者中的积累。此外,睡眠效率低下是遗传风险较低的个体发展为临床前阿尔茨海默病的潜在途径。要点 在认知能力未受损的老年人中,自我报告的睡眠与大脑淀粉样β(Aβ)的积累有关。在各种睡眠特征中,这种关系因载脂蛋白E(APOE)基因型而异。在 APOE ε4 携带者中,睡眠时间<6 小时与大脑淀粉样蛋白 beta 的快速积累有关。睡眠效率<65%与APOE ε4非携带者大脑Aβ积累速度加快有关。应研究个性化的睡眠干预措施是否有可能减缓Aβ的积累。
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