Mueller Christina, Nenert Rodolphe, Catiul Corina, Pilkington Jennifer, Szaflarski Jerzy P, Amara Amy W
Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Brain Commun. 2024 Jul 19;6(4):fcae245. doi: 10.1093/braincomms/fcae245. eCollection 2024.
Sleep deficits are a possible risk factor for development of cognitive decline and dementia in older age. Research suggests that neuroinflammation may be a link between the two. This observational, cross-sectional study evaluated relationships between sleep architecture, neuroinflammation and cognitive functioning in healthy older adults. Twenty-two adults aged ≥60 years underwent whole-brain magnetic resonance spectroscopic imaging ( method of visualizing increased brain temperatures as a proxy for neuroinflammation), supervised laboratory-based polysomnography, and comprehensive neurocognitive testing. Multiple regressions were used to assess relationships between magnetic resonance spectroscopic imaging-derived brain temperature and metabolites related to inflammation (choline; -inositol; -acetylaspartate), sleep efficiency, time and % N3 sleep and cognitive performance. Choline, -inositol and -acetylaspartate were associated with sleep efficiency and cognitive performance. Higher choline and -inositol in the bilateral frontal lobes were associated with slower processing speed and lower sleep efficiency. Higher choline and -inositol in bilateral frontoparietal regions were associated with better cognitive performance. Higher -acetylaspartate around the temporoparietal junction and adjacent white matter was associated with better visuospatial function. Brain temperature was not related to cognitive or sleep outcomes. Our findings are consistent with the limited literature regarding neuroinflammation and its relationships with sleep and cognition in older age, which has implicated ageing microglia and astrocytes in circadian dysregulation, impaired glymphatic clearance and increased blood-brain barrier integrity, with downstream effects of neurodegeneration and cognitive decline. Inflammatory processes remain difficult to measure in the clinical setting, but magnetic resonance spectroscopic imaging may serve as a marker of the relationship between neuroinflammation, sleep and cognitive decline in older adults.
睡眠不足可能是老年人认知能力下降和患痴呆症的一个风险因素。研究表明，神经炎症可能是两者之间的联系。这项观察性横断面研究评估了健康老年人的睡眠结构、神经炎症与认知功能之间的关系。22名年龄≥60岁的成年人接受了全脑磁共振波谱成像（将大脑温度升高作为神经炎症替代指标的可视化方法）、基于实验室的多导睡眠监测以及全面的神经认知测试。多元回归用于评估磁共振波谱成像得出的脑温与炎症相关代谢物（胆碱；肌醇；N-乙酰天门冬氨酸）、睡眠效率、睡眠时间和N3睡眠百分比以及认知表现之间的关系。胆碱、肌醇和N-乙酰天门冬氨酸与睡眠效率和认知表现相关。双侧额叶中较高的胆碱和肌醇与处理速度较慢和睡眠效率较低有关。双侧额顶叶区域中较高的胆碱和肌醇与较好的认知表现有关。颞顶叶交界处及相邻白质周围较高的N-乙酰天门冬氨酸与较好的视觉空间功能有关。脑温与认知或睡眠结果无关。我们的研究结果与关于神经炎症及其与老年人睡眠和认知关系的有限文献一致，这些文献表明衰老的小胶质细胞和星形胶质细胞参与昼夜节律失调、淋巴系统清除受损和血脑屏障完整性增加，具有神经退行性变和认知能力下降的下游效应。炎症过程在临床环境中仍然难以测量，但磁共振波谱成像可能作为老年人神经炎症、睡眠和认知能力下降之间关系的一个标志物。
