Tang Shi, Liu Rui, Ren Juan, Song Lin, Dong Lingling, Qin Yu, Zhao Mingqing, Wang Yongxiang, Dong Yi, Zhao Tong, Liu Cuicui, Hou Tingting, Cong Lin, Sindi Shireen, Winblad Bengt, Du Yifeng, Qiu Chengxuan
Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, China.
Department of Neurology, Shandong Provincial Hospital, Shandong University, Jinan 250021, China.
Brain Commun. 2024 Apr 26;6(3):fcae144. doi: 10.1093/braincomms/fcae144. eCollection 2024.
The neuropathological mechanisms underlying the association between sleep duration and mild cognitive impairment remain poorly understood. This population-based study included 2032 dementia-free people (age ≥ 60 years; 55.1% women) derived from participants in the Multimodal Interventions to Delay Dementia and Disability in Rural China; of these, data were available in 841 participants for Alzheimer's plasma biomarkers (e.g. amyloid-β, total tau and neurofilament light chain), 1044 for serum microvascular biomarkers (e.g. soluble adhesion molecules) and 834 for brain MRI biomarkers (e.g. whiter matter, grey matter, hippocampus, lacunes, enlarged perivascular spaces and white matter hyperintensity WMH). We used electrocardiogram-based cardiopulmonary coupling analysis to measure sleep duration, a neuropsychological test battery to assess cognitive function and the Petersen's criteria to define mild cognitive impairment. Data were analysed with multivariable logistic and general linear models. In the total sample ( = 2032), 510 participants were defined with mild cognitive impairment, including 438 with amnestic mild cognitive impairment and 72 with non-amnestic mild cognitive impairment. Long sleep duration (>8 versus 6-8 h) was significantly associated with increased likelihoods of mild cognitive impairment and non-amnestic mild cognitive impairment and lower scores in global cognition, verbal fluency, attention and executive function (Bonferroni-corrected < 0.05). In the subsamples, long sleep duration was associated with higher plasma amyloid-β40 and total tau, a lower amyloid-β42/amyloid-β40 ratio and smaller grey matter volume (Bonferroni-corrected < 0.05). Sleep duration was not significantly associated with serum-soluble adhesion molecules, white matter hyperintensity volume, global enlarged perivascular spaces and lacunes ( > 0.05). Alzheimer's and neurodegenerative pathologies may represent common pathways linking long sleep duration with mild cognitive impairment and low cognition in older adults.
睡眠时长与轻度认知障碍之间关联背后的神经病理学机制仍未得到充分理解。这项基于人群的研究纳入了来自中国农村延缓痴呆和残疾多模式干预研究参与者中的2032名无痴呆症患者（年龄≥60岁；女性占55.1%）；其中，841名参与者有阿尔茨海默病血浆生物标志物（如淀粉样蛋白-β、总tau蛋白和神经丝轻链）的数据，1044名有血清微血管生物标志物（如可溶性黏附分子）的数据，834名有脑磁共振成像生物标志物（如白质、灰质、海马体、腔隙、血管周围间隙扩大和白质高信号WMH）的数据。我们使用基于心电图的心肺耦合分析来测量睡眠时长，用一套神经心理学测试来评估认知功能，并采用彼得森标准来定义轻度认知障碍。数据通过多变量逻辑回归模型和一般线性模型进行分析。在总样本（n = 2032）中，510名参与者被定义为轻度认知障碍，其中438名是遗忘型轻度认知障碍，72名是非遗忘型轻度认知障碍。长睡眠时长（>8小时与6 - 8小时相比）与轻度认知障碍和非遗忘型轻度认知障碍的发生可能性增加以及整体认知、语言流畅性、注意力和执行功能得分较低显著相关（经邦费罗尼校正，P < 0.05）。在子样本中，长睡眠时长与血浆淀粉样蛋白-β40和总tau蛋白水平较高、淀粉样蛋白-β42/淀粉样蛋白-β40比值较低以及灰质体积较小相关（经邦费罗尼校正，P < 0.05）。睡眠时长与血清可溶性黏附分子、白质高信号体积、整体血管周围间隙扩大和腔隙无显著关联（P > 0.05）。阿尔茨海默病和神经退行性病变可能是将长睡眠时长与老年人轻度认知障碍和低认知联系起来的共同途径。
