Evidence map›Paper›PMID 39877089›Full record

ArticleResearch square2025

Cerebrospinal Fluid (CSF) Proteomic Signature in Preclinical and Clinical Alzheimer's disease (AD): Role of Adhesion Molecules.

Reem Neal, Zhiyi Yang, Malik Obideen, Melissa Peterson, Amil Shah, Ihab Hajjar

Abstract readPreprint
In one paragraph

Article in Research square, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Reem NealDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA 75390.
Zhiyi YangDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA 75390.ORCID https://orcid.org/0000-0001-6631-5513
Malik ObideenDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA 75390.
Melissa PetersonFamily Medicine and Osteopathic Manipulative Medicine, Texas College of Osteopathic Medicine, The University of North Texas Health Science Center.
Amil ShahDepartment of Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA, 75390.
Ihab HajjarDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA 75390.

Funding

The role of the renin-angiotensin-endothelial pathway in ADRF1AG051633 · NIA · EMORY UNIVERSITY · PI HAJJAR, IHAB M, QUYYUMI, ARSHED A · 2015 to 2017
$6.0M
Building a high-resolution multi-omic AD interactome with the AMP-AD and M2OVE-AD ProjectsRF1AG057470 · NIA · EMORY UNIVERSITY · PI HAJJAR, IHAB M, SEYFRIED, NICHOLAS THOMAS · 2017 to 2017
$3.1M
Hypertension, angiotensin receptor blockers, and cognition: effects and mechanismR01AG042127 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HAJJAR, IHAB M · 2012 to 2017
$3.0M
Mid-Career Program for Vascular Contributions to Alzheimer's diseaseK24AG062786 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HAJJAR, IHAB M · 2020 to 2024
$915k
NIA NIH HHS K24 AG062786NIA NIH HHS R01 AG042127NIA NIH HHS RF1 AG051633NIA NIH HHS RF1 AG057470
6 · The paper itself

Abstract

Background: Although Amyloid-beta and Tau are the hallmarks of Alzheimer's Disease (AD), other protein pathways such as endothelial dysfunction may be involved and may precede cognitive symptoms. Our objective was to characterize the cerebrospinal fluid (CSF) proteomic profiles focusing on cardiometabolic-related protein pathways in individuals on the AD spectrum. Methods: We performed CSF and plasma-targeted proteomics (276 proteins) from 354 participants of the Brain Stress Hypertension and Aging Program (BSHARP), of which 8% had preclinical AD, and 24% had MCI due to AD. We instituted a bioinformatic pipeline to generate data-driven protein modules, used "Hub" and "Critical" proteins within each module to describe protein signatures for each AD stage and then assessed their associations with clinical and biological AD traits. Finally, we completed pathway enrichment analysis to get insight into pathways that might be implicated in AD pathogenesis. Results: The 276 measured proteins clustered into five modules that were associated with CSF Amyloid-β42, Tau, and pTau. (all Conclusion: Our results suggest a proteomic signature in the CSF of individuals with preclinical AD that is driven by adhesion molecules and might be implicated in the pathogenesis of AD. Future studies investigating these pathways may provide insights into novel AD biomarkers and therapeutic targets.

Identifiers

PMID39877089
PMCPMC11774469

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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 OpenQuestion graph.