Slow-Wave Sleep and MRI Markers of Brain Aging in a Community-Based Sample
Slow-Wave Sleep and MRI Markers of Brain Aging in a Community-Based Sample
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DOI：
10.1212/wnl.0000000000011377
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发表时间：
2021-03-09
期刊：
影响因子：
9.9
通讯作者：
Himali, Jayandra J.
中科院分区：
文献类型：
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作者：
Baril, Andree-Ann;Beiser, Alexa S.;Himali, Jayandra J.
目的为了检验慢波睡眠或 N3 睡眠（被认为是睡眠恢复功能的基础）减少与大脑衰老的 MRI 标志物相关的假设，我们使用多导睡眠图和脑 MRI 评估了基于社区的弗雷明汉心脏研究后代队列中的这种关系。方法我们研究了 492 名没有神经系统疾病的参与者（年龄 58.8 +/- 8.8 岁，49.4% 男性），他们完成了脑 MRI 扫描并在家过夜多导睡眠图评估慢波睡眠（绝对持续时间和总睡眠百分比）。研究全脑、总皮质、额叶皮质、皮质下灰质、海马和白质高信号的体积占颅内体积的百分比，并评估隐性脑梗塞的存在。线性和逻辑回归模型根据年龄、年龄平方、性别、多导睡眠图和 MRI 之间的时间间隔（3.3 +/- 1.0 年）、APOE epsilon 4 携带者状态、中风危险因素、安眠药使用、体重指数和抑郁进行调整。结果慢波睡眠较少与皮质脑容量较低相关（绝对持续时间，β [标准误差] = 0.20 [0.08]，p = 0.015；百分比， 0.16 [0.08]，p = 0.044），皮质下脑体积较低（百分比，0.03 [0.02]，p = 0.034），白质高信号体积较高（绝对持续时间，-0.12 [0.05]，p = 0.010；百分比，-0.10 [0.04]，p = 0.033）。慢波睡眠持续时间与海马体积或隐性脑梗死的存在无关。结论慢波睡眠的丧失可能会加速大脑老化，其与提示脑萎缩和损伤的 MRI 标记物的关联证明了这一点。另外，轻微的损伤和加速衰老可能会降低大脑产生慢波睡眠的能力。
ObjectiveTo test the hypothesis that reduced slow-wave sleep, or N3 sleep, which is thought to underlie the restorative functions of sleep, is associated with MRI markers of brain aging, we evaluated this relationship in the community-based Framingham Heart Study Offspring cohort using polysomnography and brain MRI.MethodsWe studied 492 participants (age 58.8 +/- 8.8 years, 49.4% male) free of neurological diseases who completed a brain MRI scan and in-home overnight polysomnography to assess slow-wave sleep (absolute duration and percentage of total sleep). Volumes of total brain, total cortical, frontal cortical, subcortical gray matter, hippocampus, and white matter hyperintensities were investigated as a percentage of intracranial volume, and the presence of covert brain infarcts was evaluated. Linear and logistic regression models were adjusted for age, age squared, sex, time interval between polysomnography and MRI (3.3 +/- 1.0 years), APOE epsilon 4 carrier status, stroke risk factors, sleeping pill use, body mass index, and depression.ResultsLess slow-wave sleep was associated with lower cortical brain volume (absolute duration, beta [standard error] = 0.20 [0.08], p = 0.015; percentage, 0.16 [0.08], p = 0.044), lower subcortical brain volume (percentage, 0.03 [0.02], p = 0.034), and higher white matter hyperintensities volume (absolute duration, -0.12 [0.05], p = 0.010; percentage, -0.10 [0.04], p = 0.033). Slow-wave sleep duration was not associated with hippocampal volume or the presence of covert brain infarcts.ConclusionLoss of slow-wave sleep might facilitate accelerated brain aging, as evidence by its association with MRI markers suggestive of brain atrophy and injury. Alternatively, subtle injuries and accelerated aging might reduce the ability of the brain to produce slow-wave sleep.