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Updated: Jun 18, 2025
Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
No association between markers of systemic inflammation and endothelial dysfunction with Alzheimer's disease
Arne van Setten1, Jeroen F Uleman2, René J F Melis1
1Department of Geriatric Medicine, Radboudumc Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
Introduction:
Systemic inflammation and endothelial dysfunction are potentially modifiable factors implicated in Alzheimer's disease (AD), which offer potential therapeutic targets to slow disease progression.
Methods:
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.
Results:
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.
Discussion:
Our results do not support the role of systemic inflammation or endothelial dysfunction in progression in persons with AD.
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