Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
Sleep. 2018 May 1;41(5). doi: 10.1093/sleep/zsy025.
To investigate the cumulative effect of five consecutive nights of partial sleep deprivation (PSD) on a panel of cerebrospinal fluid (CSF) biomarkers in healthy adults.
A randomized, cross-over study conducted at the University of Gothenburg. The participants (N = 13) were healthy adults (20-40 years of age) with a normal sleeping pattern. The participants underwent a baseline sleep period consisting of five nights with 8 hr spent in bed. A subsequent period with PSD consisted of five nights of maximum 4 hr of sleep per night. Four participants were also subjected to a prolonged period of PSD consisting of eight nights with 4 hr of sleep per night. Sleep was monitored by means of observation, actigraphy, and continuous polysomnographic recordings. CSF samples were collected by routine lumbar puncture after each period. CSF biomarkers included the 38, 40, and 42 amino acid-long Aβ isoforms, total-τ, phospho-τ, orexin, monoamine metabolites (3-methoxy-4-hydroxyphenylglycol, homovanillinic acid, and 5-hydroxyindoleacetic acid), neuron-derived biomarkers (neurofilament light, neuron-specific enolase, and fatty acid-binding protein), and astro- and microglia-derived biomarkers (glial fibrillary acidic protein, S-100B, and YKL-40).
PSD was associated with a 27 per cent increase in CSF orexin concentrations (p = 0.001). No PSD-related changes in CSF biomarkers for amyloid build-up in the brain, Alzheimer's disease (AD)-type neurodegeneration, or astroglial activation were observed. PSD led to a shortening of time spent in all sleep stages except slow-wave sleep (SWS).
Five to eight consecutive nights of PSD, with preserved SWS, increased CSF orexin but had no effect on CSF biomarkers for amyloid deposition, neuronal injury, and astroglial activation.
研究连续五晚部分睡眠剥夺（PSD）对健康成年人脑脊液（CSF）生物标志物的累积影响。
这是在哥德堡大学进行的一项随机、交叉研究。参与者（N=13）为健康成年人（20-40 岁），具有正常的睡眠模式。参与者经历了一个由五晚组成的基线睡眠期，在床上度过 8 小时。随后的 PSD 期由每晚最多 4 小时的睡眠组成。有四名参与者还接受了长达八晚的 PSD 期，每晚睡眠时间为 4 小时。通过观察、活动记录仪和连续多导睡眠图记录来监测睡眠。每次睡眠期结束后，通过常规腰椎穿刺采集 CSF 样本。CSF 生物标志物包括 38、40 和 42 个氨基酸长的 Aβ 同种型、总τ、磷酸化τ、食欲素、单胺代谢物（3-甲氧基-4-羟基苯乙二醇、高香草酸和 5-羟色胺）、神经元衍生生物标志物（神经丝轻链、神经元特异性烯醇化酶和脂肪酸结合蛋白）以及星形胶质细胞和小胶质细胞衍生生物标志物（胶质纤维酸性蛋白、S-100B 和 YKL-40）。
PSD 导致 CSF 食欲素浓度增加 27%（p=0.001）。未观察到 PSD 与脑内淀粉样蛋白沉积、阿尔茨海默病（AD）型神经退行性变或星形胶质细胞激活相关的 CSF 生物标志物变化。PSD 导致除慢波睡眠（SWS）外所有睡眠阶段的时间缩短。
连续五晚至八晚 PSD，保留 SWS，增加 CSF 食欲素，但对 CSF 生物标志物无影响，如淀粉样蛋白沉积、神经元损伤和星形胶质细胞激活。
