Neurofluid coupling during sleep and wake states.
Neurofluid coupling during sleep and wake states.
复制标题
睡眠和清醒状态下的神经流体耦合。
DOI：
10.1016/j.sleep.2023.07.021
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发表时间：
2023
期刊：
影响因子：
4.8
通讯作者：
Schwichtenberg,AJ
中科院分区：
文献类型：
--
作者：
VijayakrishnanNair,Vidhya;Kish,BriannaR;Chong,PearlynneLh;Yang,Ho-ChingShawn;Wu,Yu-Chien;Tong,Yunjie;Schwichtenberg,AJ
背景在临床人群中，睡眠期间脑脊液（CSF）的运动是一个不断增长的研究领域，在神经退行性疾病（例如，阿尔茨海默病）和神经发育障碍。然而，我们对影响CSF运动的过程知之甚少。为了告知临床干预目标，本研究评估了（a）实时CSF运动、（B）神经元驱动的运动和（c）非神经元系统生理驱动的运动之间的耦合。和非神经元系统生理学与外周功能近红外光谱（fNIRS）。暂时评估神经元和非神经元驱动器;其中，EEG测量的在CSF运动之前的慢波活动被认为是神经元驱动的。同样，慢波振荡（通过fNIRS评估），加上CSF运动被认为是非神经元的全身生理学driven.Results and conclusionsOur结果文件神经的CSF运动的贡献只存在于轻NREM睡眠，但低频非神经元振荡强烈耦合CSF运动在所有评估状态-清醒，NREM-1，NREM-2。这些发现的临床/研究意义是双重的。首先，神经元驱动的振荡有助于深度睡眠（NREM-3）之外的CSF运动;因此，旨在增加CSF运动的干预措施可能会产生有意义的增加，更普遍地促进NREM睡眠-可能不需要关注NREM S3。第二，非神经元系统振荡在清醒和睡眠阶段起作用;因此，干预可能通过操纵全身生理学来增加CSF运动。
BackgroundIn clinical populations, the movement of cerebrospinal fluid (CSF) during sleep is a growing area of research with potential mechanistic connections in both neurodegenerative (e.g., Alzheimer's Disease) and neurodevelopmental disorders. However, we know relatively little about the processes that influence CSF movement. To inform clinical intervention targets this study assesses the coupling between (a) real-time CSF movement, (b) neuronal-driven movement, and (c) non-neuronal systemic physiology driven movement.MethodsThis study included eight young, healthy volunteers, with concurrently acquired neurofluid dynamics using functional Magnetic Resonance Imaging (MRI), neural activity using Electroencephalography (EEG), and non-neuronal systemic physiology with peripheral functional Near-Infrared Spectroscopy (fNIRS). Neuronal and non-neuronal drivers were assessed temporally; wherein, EEG measured slow wave activity that preceded CSF movement was considered neuronally driven. Similarly, slow wave oscillations (assessed via fNIRS) that coupled with CSF movement were considered non-neuronal systemic physiology driven.Results and conclusionsOur results document neural contributions to CSF movement were only present during light NREM sleep but low-frequency non-neuronal oscillations were strongly coupled with CSF movement in all assessed states – awake, NREM-1, NREM-2. The clinical/research implications of these findings are two-fold. First, neuronal-driven oscillations contribute to CSF movement outside of deep sleep (NREM-3); therefore, interventions aimed at increasing CSF movement may yield meaningful increases with the promotion of NREM sleep more generally – a focus on NREM S3 may not be needed. Second, non-neuronal systemic oscillations contribute across wake and sleep stages; therefore, interventions may increase CSF movement by manipulating systemic physiology.