The mechanism underlying the possible causal association between long-term sleep disruption and Alzheimer’s disease remains unclear Musiek et al. 2015. A hypothesised pathway through increased brain amyloid load was not confirmed in previous work in our cohort of maritime pilots with long-term work-related sleep disruption Thomas et al. Alzheimer’s Res Ther 2020;12:101. Here, using functional MRI, T2-FLAIR, and arterial spin labeling MRI scans, we explored alternative neuroimaging biomarkers related to both sleep disruption and AD: resting-state network co-activation and between-network connectivity of the default mode network (DMN), salience network (SAL) and frontoparietal network (FPN), vascular damage and cerebral blood flow (CBF). We acquired data of 16 maritime pilots (56 ± 2.3 years old) with work-related long-term sleep disruption (23 ± 4.8 working years) and 16 healthy controls (59 ± 3.3 years old), with normal sleep patterns (Pittsburgh Sleep Quality Index ≤ 5). Maritime pilots did not show altered co-activation in either the DMN, FPN, or SAL and no differences in between-network connectivity. We did not detect increased markers of vascular damage in maritime pilots, and additionally, maritime pilots did not show altered CBF-patterns compared to healthy controls. In summary, maritime pilots with long-term sleep disruption did not show neuroimaging markers indicative of preclinical AD compared to healthy controls. These findings do not resemble those of short-term sleep deprivation studies. This could be due to resiliency to sleep disruption or selection bias, as participants have already been exposed to and were able to deal with sleep disruption for multiple years, or to compensatory mechanisms Mentink et al. PLoS ONE. 2021;15(12):e0237622. This suggests the relationship between sleep disruption and AD is not as strong as previously implied in studies on short-term sleep deprivation, which would be beneficial for all shift workers suffering from work-related sleep disruptions.

长期睡眠中断与阿尔茨海默病之间可能因果关系的机制仍不清楚 Musiek 等人，2015 年。在我们之前的工作中，通过增加大脑淀粉样蛋白负荷的假设途径在我们之前的工作中没有得到证实，这些飞行员长期与工作相关的睡眠中断 Thomas 等人。阿尔茨海默氏症研究 2020;12：101。在这里，使用功能性 MRI、T2-FLAIR 和动脉自旋标记 MRI 扫描，我们探索了与睡眠中断和 AD 相关的替代神经影像学生物标志物：默认模式网络 （DMN）、显著性网络 （SAL） 和额顶叶网络 （FPN） 的静息态网络共同激活和网络间连接，血管损伤和脑血流 （CBF）。我们获取了 16 名与工作相关的长期睡眠中断 （23 ± 4.8 工作年） 的海上飞行员 （56 ± 2.3 岁） 和 16 名健康对照 （59 ± 3.3 岁），睡眠模式正常 （匹兹堡睡眠质量指数 ≤ 5）。海事飞行员在 DMN 、 FPN 或 SAL 中没有表现出改变的共激活，并且在网络连接方面没有差异。我们没有检测到海事飞行员血管损伤标志物的增加，此外，与健康对照组相比，海事飞行员没有表现出 CBF 模式的改变。总之，与健康对照相比，长期睡眠中断的海上飞行员没有显示指示临床前 AD 的神经影像学标志物。这些发现与短期睡眠剥夺研究的结果不同。这可能是由于对睡眠中断的弹性或选择偏倚，因为参与者已经暴露并能够处理睡眠中断多年，或者是由于补偿机制 Mentink et al. PLoS ONE。2021;15（12）：e0237622。 这表明睡眠中断与 AD 之间的关系并不像之前关于短期睡眠剥夺的研究中暗示的那样强烈，这对所有遭受与工作相关的睡眠中断的轮班工人都是有益的。