Healthy Brain Ageing Program, Brain and Mind Centre, University of Sydney, Sydney, New South Wales, Australia.
Faculty of Science, School of Psychology, University of Sydney, Sydney, New South Wales, Australia.
Eur J Neurol. 2024 Dec;31(12):e16491. doi: 10.1111/ene.16491. Epub 2024 Sep 20.
Obstructive sleep apnea is associated with increased dementia risk. Nocturnal hypoxemia, which can be more severe during rapid eye movement (REM) sleep, may be a key mechanism. This study examines how REM hypoxemia affects memory and explores whether hippocampal vulnerability to hypoxemia mediates this effect in older adults at risk for dementia.
Older adults aged ≥50 years (N = 338) with subjective or mild cognitive impairment (i.e., objective impairment) underwent neuropsychological, mood, and medical assessment, magnetic resonance imaging scanning (n = 135), and overnight polysomnography. Verbal learning and memory were assessed with the Rey Auditory Verbal Learning Test. REM sleep hypoxemia was measured using the Oxygen Desaturation Index-3% (REM-ODI). Hippocampal subfield (CA1, CA3, subiculum, and dentate gyrus) volumes were derived from T1 and high-resolution hippocampus T2 scans. We determined whether the relationship between REM-ODI and learning and memory was mediated by hippocampal subfield volume. Analyses were repeated in non-REM sleep to determine whether the effects were REM-specific.
Although there was not a direct effect of REM-ODI on verbal learning (p > 0.05) or memory (p > 0.05), mediation analyses showed a significant indirect effect of high REM-ODI on poorer verbal learning (β = -0.09, 95% confidence interval [CI] = -0.238 to -0.005) and memory (β = -0.100, 95% CI = -0.255 to -0.005), which was mediated by CA1 volume. These associations were absent in non-REM sleep (p > 0.05).
Hypoxemia during REM sleep may impair memory in people at risk for dementia by reducing CA1 hippocampal volume. Research is needed to explore whether interventions targeting REM sleep hypoxemia are protective against memory decline.
阻塞性睡眠呼吸暂停与痴呆风险增加有关。在快速眼动（REM）睡眠期间可能更为严重的夜间低氧血症可能是一个关键机制。本研究探讨了 REM 低氧血症如何影响记忆，并探索了海马体对低氧血症的脆弱性是否在有痴呆风险的老年人中介导了这种影响。
年龄在 50 岁及以上（N=338）有主观或轻度认知障碍（即客观障碍）的老年人接受了神经心理学、情绪和医学评估、磁共振成像扫描（n=135）和整夜多导睡眠图。使用 Rey 听觉言语学习测试评估言语学习和记忆。使用 REM 低氧指数-3%（REM-ODI）测量 REM 睡眠低氧血症。从 T1 和高分辨率海马体 T2 扫描中得出海马体亚区（CA1、CA3、下托和齿状回）体积。我们确定了 REM-ODI 与学习和记忆之间的关系是否由海马体亚区体积介导。在非 REM 睡眠中重复了分析，以确定这些影响是否是 REM 特异性的。
尽管 REM-ODI 对言语学习（p>0.05）或记忆（p>0.05）没有直接影响，但中介分析显示 REM-ODI 与较差的言语学习（β=-0.09，95%置信区间[CI] = -0.238 至 -0.005）和记忆（β=-0.100，95% CI = -0.255 至 -0.005）之间存在显著的间接影响，这是由 CA1 体积介导的。这些关联在非 REM 睡眠中不存在（p>0.05）。
REM 睡眠期间的低氧血症可能通过减少 CA1 海马体体积而损害痴呆风险人群的记忆。需要研究是否针对 REM 睡眠低氧血症的干预措施可以预防记忆下降。
