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携带者中的内皮祖细胞与脑小血管病

Endothelial progenitor cells and cerebral small vessel disease in carriers.

作者信息

Kapoor Arunima, Dutt Shubir, Nguyen Amy, Lohman Trevor, Gaubert Aimée, Alitin John Paul M, Sible Isabel J, Marshall Anisa, Shenasa Fatemah, Engstrom Allison C, Bradford David Robert, Rodgers Kathleen, Nation Daniel A

机构信息

Department of Psychological Science, University of California, Irvine, Irvine, CA, USA.

Department of Psychology, University of Southern California, Los Angeles, CA, USA.

出版信息

Cereb Circ Cogn Behav. 2025 Feb 11;8:100378. doi: 10.1016/j.cccb.2025.100378. eCollection 2025.

DOI:10.1016/j.cccb.2025.100378
PMID:40034682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11872604/
Abstract

carriers at genetic risk for Alzheimer's disease exhibit early cerebrovascular dysfunction, which may be triggered by endothelial dysfunction. Endothelial progenitor cells (EPCs) represent cell populations involved in promoting angiogenesis and facilitating vascular repair in response to injury. We examined whether elevated EPCs are associated with lower cerebral small vessel disease burden in carriers prior to cognitive decline. Independently living older adults ( = 109, mean age = 70.5 years; SD = 7.9; 34.9 % male) free of dementia or clinical stroke underwent brain MRI and venipuncture. Small vessel disease was determined using a validated scale. White matter hyperintensity (WMH) volume was determined using the lesion segmentation toolbox. PBMCs were cultured and EPCs were defined as number of colony forming units in vitro. Regression analysis revealed an association between average number of EPC colonies and lower small vessel disease load ( = .026) and WMH volume ( = .002), in carriers. Findings suggest that EPC colony count may indicate activation of mechanisms which protect cerebrovascular function in carriers prior to the development of cognitive decline.

摘要

有患阿尔茨海默病遗传风险的携带者表现出早期脑血管功能障碍,这可能由内皮功能障碍引发。内皮祖细胞(EPCs)代表参与促进血管生成和促进损伤后血管修复的细胞群体。我们研究了在认知衰退之前,EPCs升高是否与携带者较低的脑小血管疾病负担相关。独立生活的无痴呆或临床中风的老年人(n = 109,平均年龄 = 70.5岁;标准差 = 7.9;34.9%为男性)接受了脑部MRI和静脉穿刺。使用经过验证的量表确定小血管疾病。使用病变分割工具箱确定白质高信号(WMH)体积。培养外周血单核细胞(PBMCs),并将EPCs定义为体外集落形成单位的数量。回归分析显示,在携带者中,EPC集落的平均数量与较低的小血管疾病负荷(P = .026)和WMH体积(P = .002)之间存在关联。研究结果表明,EPC集落计数可能表明在认知衰退发生之前,保护携带者脑血管功能的机制被激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24f2/11872604/8e5125a444cc/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24f2/11872604/7b2b039d5fcb/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24f2/11872604/8e5125a444cc/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24f2/11872604/7b2b039d5fcb/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24f2/11872604/8e5125a444cc/gr2.jpg

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ApoE (Apolipoprotein E) in Brain Pericytes Regulates Endothelial Function in an Isoform-Dependent Manner by Modulating Basement Membrane Components.载脂蛋白 E(Apolipoprotein E)在脑周细胞中通过调节基底膜成分以依赖于亚型的方式调节内皮功能。
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