Evidence map›Paper›PMID 39085534›Full record

ArticleGeroScience2025

No association between markers of systemic inflammation and endothelial dysfunction with Alzheimer's disease progression: a longitudinal study.

Arne van Setten, Jeroen F Uleman, René J F Melis, Brian Lawlor, Niels P Riksen, Jurgen A H R Claassen, Rianne A A de Heus, NILVAD Study Group

Abstract read
In one paragraph

Article in GeroScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Arne van Setten *Department of Geriatric Medicine, Radboudumc Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
Jeroen F Uleman *Copenhagen Health Complexity Center, Department of Public Health, University of Copenhagen, Oster Farimagsgade 5, 1353, Copenhagen K, Denmark. jeroen.uleman@sund.ku.dk.ORCID 0000-0001-5050-8505
René J F MelisDepartment of Geriatric Medicine, Radboudumc Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
Brian LawlorGlobal Brain Health Institute, Trinity College, Dublin, Ireland.
Niels P RiksenDepartment of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
Jurgen A H R ClaassenDepartment of Geriatric Medicine, Radboudumc Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
Rianne A A de HeusDepartment of Geriatric Medicine, Radboudumc Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
NILVAD Study Group

Funding

Alzheimer's Drug Discovery Foundation 20121210Seventh Framework Programme 279093ZonMw 04520232320007
6 · The paper itself

Abstract

introductionSystemic inflammation and endothelial dysfunction are potentially modifiable factors implicated in Alzheimer's disease (AD), which offer potential therapeutic targets to slow disease progression.

methodsWe 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.

resultsThe 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.

Indexed as

Alzheimer DiseaseEndothelium, VascularInflammationAgedAged, 80 and overBiomarkersCognitive DysfunctionDisease ProgressionE-SelectinFemaleHumansIntercellular Adhesion Molecule-1Longitudinal StudiesMaleTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1BiomarkersE-SelectinIntercellular Adhesion Molecule-1Tumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1ADAS-cogAlzheimer’s diseaseBiomarkerCytokineEndothelial dysfunctionLongitudinalMediationMixed modelProgressionSystemic inflammation

Identifiers

PMID39085534
PMCPMC11872860

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.