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Obstructive sleep apnea and Alzheimer's disease-related cerebrospinal fluid biomarkers in mild cognitive impairment.轻度认知障碍与阻塞性睡眠呼吸暂停及阿尔茨海默病相关的脑脊液生物标志物。
Sleep. 2021 Jan 21;44(1). doi: 10.1093/sleep/zsaa133.
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Neurofilament light as a biomarker in traumatic brain injury.神经丝轻链作为创伤性脑损伤的生物标志物。
Neurology. 2020 Aug 11;95(6):e610-e622. doi: 10.1212/WNL.0000000000009983. Epub 2020 Jul 8.
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Repetitive Mild Traumatic Brain Injury Alters Glymphatic Clearance Rates in Limbic Structures of Adolescent Female Rats.反复轻度外伤性脑损伤改变青春期雌性大鼠边缘结构的神经胶质淋巴清除率。
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Plasma tau, neurofilament light chain and amyloid-β levels and risk of dementia; a population-based cohort study.血浆 tau 蛋白、神经丝轻链和淀粉样 β 水平与痴呆风险:一项基于人群的队列研究。
Brain. 2020 Apr 1;143(4):1220-1232. doi: 10.1093/brain/awaa054.
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Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men.急性睡眠缺失对年轻男性中枢神经系统健康生物标志物日间血浆动力学的影响。
Neurology. 2020 Mar 17;94(11):e1181-e1189. doi: 10.1212/WNL.0000000000008866. Epub 2020 Jan 8.
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The association of insomnia and sleep apnea with deployment and combat exposure in the entire population of US army soldiers from 1997 to 2011: a retrospective cohort investigation.1997 年至 2011 年美国军队全体士兵中失眠和睡眠呼吸暂停与部署和战斗暴露的关系:一项回顾性队列研究。
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The role of neurofilament aggregation in neurodegeneration: lessons from rare inherited neurological disorders.神经丝聚集在神经退行性变中的作用:罕见遗传性神经疾病的启示。
Mol Neurodegener. 2019 May 16;14(1):19. doi: 10.1186/s13024-019-0318-4.
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Correlates of Depression in U.S. Military Service Members With a History of Mild Traumatic Brain Injury.有轻度创伤性脑损伤病史的美国军人中抑郁症的相关因素
Mil Med. 2019 Mar 1;184(Suppl 1):148-154. doi: 10.1093/milmed/usy321.
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The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans.睡眠-觉醒周期调节小鼠脑间质液 tau 和人类 CSF tau。
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Obstructive sleep apnea treatment, slow wave activity, and amyloid-β.阻塞性睡眠呼吸暂停治疗、慢波活动与淀粉样β。
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轻度创伤性脑损伤患者的睡眠质量与神经退行性变生物标志物相关:CENC 研究。

Poor sleep correlates with biomarkers of neurodegeneration in mild traumatic brain injury patients: a CENC study.

机构信息

Department of Neurology, Uniformed Services University of Health Sciences, Bethesda, MD.

Center for Neuroscience and Regenerative Medicine, Bethesda, MD.

出版信息

Sleep. 2021 Jun 11;44(6). doi: 10.1093/sleep/zsaa272.

DOI:10.1093/sleep/zsaa272
PMID:33280032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8343591/
Abstract

STUDY OBJECTIVES

Sleep disorders affect over half of mild traumatic brain injury (mTBI) patients. Despite evidence linking sleep and neurodegeneration, longitudinal TBI-related dementia studies have not considered sleep. We hypothesized that poor sleepers with mTBI would have elevated markers of neurodegeneration and lower cognitive function compared to mTBI good sleepers and controls. Our objective was to compare biomarkers of neurodegeneration and cognitive function with sleep quality in warfighters with chronic mTBI.

METHODS

In an observational warfighters cohort (n = 138 mTBI, 44 controls), the Pittsburgh Sleep Quality Index (PSQI) was compared with plasma biomarkers of neurodegeneration and cognitive scores collected an average of 8 years after injury.

RESULTS

In the mTBI cohort, poor sleepers (PSQI ≥ 10, n = 86) had elevated plasma neurofilament light (NfL, x̅ = 11.86 vs 7.91 pg/mL, p = 0.0007, d = 0.63) and lower executive function scores by the categorical fluency (x̅ = 18.0 vs 21.0, p = 0.0005, d = -0.65) and stop-go tests (x̅ = 30.1 vs 31.1, p = 0.024, d = -0.37). These findings were not observed in controls (n = 44). PSQI predicted NfL (beta = 0.22, p = 0.00002) and tau (beta = 0.14, p = 0.007), but not amyloid β42. Poor sleepers showed higher obstructive sleep apnea (OSA) risk by STOP-BANG scores (x̅ = 3.8 vs 2.7, p = 0.0005), raising the possibility that the PSQI might be partly secondary to OSA.

CONCLUSIONS

Poor sleep is linked to neurodegeneration and select measures of executive function in mTBI patients. This supports implementation of validated sleep measures in longitudinal studies investigating pathobiological mechanisms of TBI related neurodegeneration, which could have therapeutic implications.

摘要

研究目的

睡眠障碍影响超过一半的轻度创伤性脑损伤(mTBI)患者。尽管有证据表明睡眠与神经退行性变有关,但与 TBI 相关的痴呆症的纵向研究并未考虑睡眠。我们假设与 mTBI 良好睡眠者和对照组相比,睡眠不佳的 mTBI 患者会有更高的神经退行性变标志物和更低的认知功能。我们的目的是比较慢性 mTBI 战士的睡眠质量与神经退行性变生物标志物和认知功能。

方法

在一项观察性战士队列(n = 138 例 mTBI,44 例对照)中,比较匹兹堡睡眠质量指数(PSQI)与平均受伤 8 年后采集的神经退行性变血浆生物标志物和认知评分。

结果

在 mTBI 队列中,睡眠不佳者(PSQI≥10,n = 86)的血浆神经丝轻链(NfL,x̅ = 11.86 与 7.91 pg/mL,p = 0.0007,d = 0.63)升高,且执行功能评分较低,类别流畅性(x̅ = 18.0 与 21.0,p = 0.0005,d = -0.65)和停止-走测试(x̅ = 30.1 与 31.1,p = 0.024,d = -0.37)。这些发现在对照组(n = 44)中并未观察到。PSQI 预测 NfL(β = 0.22,p = 0.00002)和 tau(β = 0.14,p = 0.007),但不预测淀粉样蛋白β42。睡眠不佳者的 STOP-BANG 评分显示阻塞性睡眠呼吸暂停(OSA)风险更高(x̅ = 3.8 与 2.7,p = 0.0005),这表明 PSQI 可能部分是由于 OSA 引起的。

结论

睡眠质量差与 mTBI 患者的神经退行性变和特定执行功能测量有关。这支持在研究与 TBI 相关神经退行性变的病理生物学机制的纵向研究中实施经过验证的睡眠测量,这可能具有治疗意义。