睡眠机制知识库

前扣带皮层兴奋-抑制平衡的睡眠依赖性改变将 BOLD-CSF 耦合变化与 OSA 认知表现相联系

Sleep-dependent alterations in anterior cingulate cortex excitation-inhibition balance link alterations in BOLD-CSF coupling to cognitive performance in obstructive sleep apnea.

原始研究开放获取
作者
Ning Y, Li Y, Xiong Z, Sheng Z, He L, Xiang S, Hu Y, Peng J, Lv F 等
期刊
Frontiers in aging neuroscience
出处
2026; 18; 1932223
DOI
10.3389/fnagi.2026.1932223
PMID
42798625

一句话摘要

87 名参与者(50 例 OSA、37 例对照)在睡眠前后各做一次 MRI 并整夜 PSG,考察前扣带皮层兴奋—抑制平衡的睡眠依赖性改变及其与 BOLD-CSF 耦合和认知表现的关系;结论:OSA 严重度与 ACC 特异性 BOLD-CSF 解耦及 ACC-GABA 夜间下降受损相关,E/I 变化幅度调节耦合与认知的关联。

为什么重要

把类淋巴功能代理指标(BOLD-CSF 耦合)与突触层面的兴奋—抑制平衡及认知表现串联起来,为 OSA 认知损害的机制提供了跨层次的人体证据。

英文摘要原文

Objective The roles of cortical glymphatic dysfunction and excitation-inhibition imbalance in cognitive impairment associated with obstructive sleep apnea (OSA) require further study. This study aimed to investigate sleep-related glymphatic function and neurotransmitter changes in OSA and their relationships with cognition. Methods Eighty seven participants (50 OSA, 37 controls) completed a pre-sleep MRI, followed by an overnight PSG recording, and a post-sleep MRI to assess sleep-dependent glymphatic and neurotransmitter changes. Resting-state blood-oxygen-level-dependent (BOLD) signals and cerebrospinal fluid (CSF) signals (BOLD-CSF coupling), an indirect glymphatic-related imaging proxy, were assessed in the global cortex, anterior cingulate cortex (ACC), posterior cingulate cortex (PCC), and default mode network (DMN) cortex. MRS-derived gamma-aminobutyric acid (GABA) and glutamate/glutamine (Glx) levels were measured in the ACC and PCC as indirect neurochemical measures of excitation-inhibition (E/I) balance. General linear models, linear mixed-effects models, correlation analyses, and moderation analyses were employed to examine group differences, overnight changes in BOLD-CSF coupling and neurotransmitters, and their relationships with cognitive performance. Results In the moderate-to-severe OSA group, pre-sleep global and ACC-BOLD-CSF coupling were weaker than in controls, and ACC-GABA showed a group × time interaction (η p 2 = 0.105, p -FDR = 0.049), with a significant overnight decrease observed only in controls (Cohen's d = 0.75, p -FDR = 0.007). Greater magnitudes of overnight change in both ACC-BOLD-CSF coupling and ACC-E/I were independently associated with worse cognition. ACC-E/I change also moderated the coupling-cognition relationship ( β = 0.590, p = 0.015), with a significant negative association only at smaller magnitudes of E/I change ( β = -0.729, p = 0.002). Conclusion Our findings suggest that OSA severity is associated with ACC-specific BOLD-CSF decoupling and a disrupted overnight decline in ACC-GABA. The magnitude of overnight E/I variation moderated the association between BOLD-CSF coupling variation and cognitive performance. These preliminary findings highlight the potential relevance of ACC-BOLD-CSF coupling and neurochemical alterations to OSA-related cognitive impairment. Future studies with larger sample sizes are needed to confirm these findings.

所属章节

突触稳态假说 类淋巴系统与代谢废物清除

兴奋抑制平衡 BOLD-CSF 耦合 认知 睡眠呼吸暂停

条目编号 P068 · 元数据经 Crossref / Europe PMC 回查