睡眠障碍:发病机制和治疗干预

IF 10.7 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
MedComm Pub Date : 2025-03-10 DOI:10.1002/mco2.70130
Cheng Liu, Zhigang He, Yanqiong Wu, Yanbo Liu, Zhixiao Li, Yifan Jia, Hongbing Xiang
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引用次数: 0

摘要

睡眠障碍严重影响患者的生活质量。虽然它在临床上是公认的,但基本的神经病理机制仍然不清楚。最近的临床前研究旨在了解睡眠剥夺和睡眠/觉醒失调的基本机制。睡眠障碍与认知神经基础的结构和功能的变化有关。基于电生理学和光遗传学/化学遗传学技术的进展,我们回顾了与睡眠障碍相关的神经回路,以及连接和脑区域功能的改变。我们随后概述了在临床前研究中与睡眠障碍相关的细胞和分子修饰,主要涉及神经元代谢、电生理活动、突触可塑性和神经胶质细胞的变化。相应的,在脑与外周器官相互作用的基础上,我们阐明了腹腔疾病和肝脏疾病参与睡眠障碍发病的潜在机制。在本文中,我们主要从分子、细胞和神经回路水平讨论了睡眠障碍的发病机制。该综述还涵盖了治疗睡眠障碍的潜在策略和未来的研究途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Sleep Disorders: Pathogenesis and Therapeutic Interventions

Sleep Disorders: Pathogenesis and Therapeutic Interventions

Sleep disorder significantly disrupts the quality of life for patients. Although it is clinically acknowledged, the fundamental neuropathological mechanisms are still not understood. Recent preclinical research has been directed toward understanding the fundamental mechanisms underlying the sleep deprivation and sleep/wake dysregulation. Sleep disorder is linked to changes in the structure and function of the neural basis of cognition. We reviewed the neural circuits related to sleep disorders, along with alterations in connectivity and brain region functions, based on advancements in electrophysiology and optogenetic/chemogenetic techniques. We subsequently outline the cellular and molecular modifications linked to sleep disorders in preclinical studies, primarily involving changes in neuronal metabolism, electrophysiological activity, synaptic plasticity, and glial cells. Correspondingly, on the basis of the crosstalk between the brain and peripheral organs, we elucidate the underlying mechanisms of the involvement of celiac disease and hepatic disease in the pathogenesis of sleep disorders. In this review, we mainly discussed the pathogenesis at molecular, cellular, and neural circuit levels that contribute to sleep disorder. The review also covered potential strategies for treating sleep disorders and future research avenues.

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来源期刊
CiteScore
6.70
自引率
0.00%
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审稿时长
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