van Setten Arne, Uleman Jeroen F, Melis René J F, Lawlor Brian, Riksen Niels P, Claassen Jurgen A H R, de Heus Rianne A A
Department of Geriatric Medicine, Radboudumc Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
Copenhagen Health Complexity Center, Department of Public Health, University of Copenhagen, Oster Farimagsgade 5, 1353, Copenhagen K, Denmark.
Geroscience. 2025 Feb;47(1):1093-1104. doi: 10.1007/s11357-024-01294-x. Epub 2024 Jul 31.
Systemic inflammation and endothelial dysfunction are potentially modifiable factors implicated in Alzheimer's disease (AD), which offer potential therapeutic targets to slow disease progression.
We investigated the relationship between baseline circulating levels of inflammatory (TNF-α, IL-1ß) and endothelial cell markers (VCAM-1, ICAM-1, E-selectin) and 18-month cognitive decline (ADAS-cog12) in 266 mild-to-moderate AD patients from the NILVAD study. We employed individual growth models to examine associations, potential mediation, and interaction effects while adjusting for confounders.
The average increase in ADAS-cog12 scores over all patients was 8.1 points in 18 months. No significant association was found between the markers and the rate of cognitive decline. Mediation analysis revealed no mediating role for endothelial cell markers, and interaction effects were not observed.
Our results do not support the role of systemic inflammation or endothelial dysfunction in progression in persons with AD.
全身炎症和内皮功能障碍是阿尔茨海默病(AD)中潜在的可改变因素,它们为减缓疾病进展提供了潜在的治疗靶点。
我们在NILVAD研究中的266例轻度至中度AD患者中,研究了炎症标志物(TNF-α、IL-1ß)和内皮细胞标志物(VCAM-1、ICAM-1、E-选择素)的基线循环水平与18个月认知衰退(ADAS-cog12)之间的关系。我们采用个体生长模型来检验关联、潜在中介和交互作用,同时对混杂因素进行校正。
所有患者的ADAS-cog12评分在18个月内平均增加8.1分。未发现标志物与认知衰退率之间存在显著关联。中介分析显示内皮细胞标志物无中介作用,也未观察到交互作用。
我们的结果不支持全身炎症或内皮功能障碍在AD患者病情进展中的作用。