乙醛功能障碍介导了炎症驱动的血管负荷和脑小血管疾病的认知能力下降
Glymphatic dysfunction mediates inflammation-driven vascular burden and cognitive decline in cerebral small vessel disease.
摘要(中文译文)
脑小血管病（CSVD）日益被认为是一种涉及微血管功能障碍、血管周围清除受损及炎症过程的疾病。然而，全身炎症负荷、神经血管耦合（NVC）、类淋巴系统MRI标志物、血管病变负荷与认知功能之间的相互关系仍不明确。在这项前瞻性研究中，155例CSVD患者和70名健康对照者（HCs）接受了多模态MRI检查。NVC通过脑血流量/低频波动分数振幅比值进行量化。类淋巴功能通过沿血管周围间隙的弥散张量图像分析（ALPS）指数、脉络丛体积（CPV）及血管周围间隙（PVS）分数进行评估。采用结构方程模型（SEM）评估炎症标志物对血管负荷和认知表现的直接与间接效应。与健康对照者相比，CSVD患者表现出显著减低的NVC（具体位于右侧中扣带回和左侧额回）以及受损的类淋巴功能（较低的ALPS指数；较高的CPV和PVS分数）。SEM显示，炎症生物标志物对血管负荷既产生直接效应，也通过两条通路产生显著的间接效应（占总效应的66.3%）：经类淋巴功能的单一中介路径（42.8%）以及经NVC和类淋巴功能的序列中介路径（23.5%）。血管负荷增加与较差的认知表现显著相关。炎症主要通过破坏NVC和类淋巴清除机制驱动CSVD进展和认知功能下降。这些发现突显了类淋巴功能障碍是炎症相关结构性脑损伤的关键中介因素。
Abstract
Cerebral small vessel disease (CSVD) is increasingly recognized as a disorder involving microvascular dysfunction, impaired perivascular clearance, and inflammatory processes. However, how systemic inflammatory burden, neurovascular coupling (NVC), glymphatic MRI markers, vascular lesion burden, and cognition are interrelated remains unclear. In this prospective study, 155 patients with CSVD and 70 healthy controls (HCs) underwent multimodal MRI. NVC was quantified using the cerebral blood flow/fractional amplitude of low-frequency fluctuations ratio. Glymphatic function was assessed via the diffusion tensor image analysis along the perivascular space (ALPS) index, choroid plexus volume (CPV), and perivascular space (PVS) fractions. Structural equation modeling (SEM) was employed to evaluate the direct and indirect effects of inflammatory markers on vascular burden and cognitive performance. Patients with CSVD exhibited significantly diminished NVC (specifically in the right median cingulate and left frontal gyri) and impaired glymphatic function (lower ALPS-index; higher CPV and PVS fractions) compared to HCs. SEM revealed that inflammatory biomarkers exerted both a direct effect on vascular burden and a substantial indirect effect (accounting for 66.3% of the total effect) mediated through two pathways: a single-mediation path via glymphatic function (42.8%) and a serial-mediation path via NVC and glymphatic function (23.5%). Increased vascular burden was significantly associated with poorer cognitive performance. Inflammation drives CSVD progression and cognitive decline primarily through the disruption of NVC and glymphatic clearance mechanisms. These findings highlight glymphatic dysfunction as a critical mediator of inflammation-related structural brain damage.
如何引用
AMA
Yilei Chen, Jiejing Zhang, Yingjie Kang, Mei Yang, Yingying Zhang, Xuying Zhu, et al. Glymphatic dysfunction mediates inflammation-driven vascular burden and cognitive decline in cerebral small vessel disease.. Neurobiology of disease. 2026; doi:10.1016/j.nbd.2026.107548.
APA
Yilei Chen, Jiejing Zhang, Yingjie Kang, Mei Yang, Yingying Zhang, Xuying Zhu, et al (2026). Glymphatic dysfunction mediates inflammation-driven vascular burden and cognitive decline in cerebral small vessel disease.. Neurobiology of disease. https://doi.org/10.1016/j.nbd.2026.107548
GB/T 7714
Yilei Chen, Jiejing Zhang, Yingjie Kang, Mei Yang, Yingying Zhang, Xuying Zhu, et al. Glymphatic dysfunction mediates inflammation-driven vascular burden and cognitive decline in cerebral small vessel disease.[J]. Neurobiology of disease, 2026 doi:10.1016/j.nbd.2026.107548.
在 PubMed增强版 阅读全文
翻译全文 · AI 文献问答 · PDF 原文下载 · 引用导出