Evidence map›Paper›PMID 38570813›Full record

ArticleImmunity & ageing : I & A2024

Addition of inflammation-related biomarkers to the CAIDE model for risk prediction of all-cause dementia, Alzheimer's disease and vascular dementia in a prospective study.

Kira Trares, Manuel Wiesenfarth, Hannah Stocker, Laura Perna, Agnese Petrera, Stefanie M Hauck, Konrad Beyreuther, Hermann Brenner, Ben Schöttker

Open access · goldAbstract read
In one paragraph

Article in Immunity & ageing : I & A, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% of its field
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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
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

9 authors at 4 institutions in 1 country.

Kira TraresDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center, Im Neuenheimer Feld 581, Heidelberg, 69120, Germany.
Manuel WiesenfarthDivision of Biostatistics, German Cancer Research Center, Heidelberg, Germany.
Hannah StockerDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center, Im Neuenheimer Feld 581, Heidelberg, 69120, Germany.
Laura PernaDepartment of Genes and Environment, Max Planck Institute of Psychiatry, Kraepelinstraße 2-10, Munich, 80804, Germany.
Agnese PetreraMetabolomics and Proteomics Core, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Stefanie M HauckMetabolomics and Proteomics Core, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Konrad BeyreutherNetwork Aging Research, Heidelberg University, Bergheimer Straße 20, Heidelberg, 69115, Germany.
Hermann BrennerDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center, Im Neuenheimer Feld 581, Heidelberg, 69120, Germany.
Ben SchöttkerDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center, Im Neuenheimer Feld 581, Heidelberg, 69120, Germany. b.schoettker@dkfz.de.
Heidelberg University · DEGerman Cancer Research Center · DEHelmholtz Zentrum München · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is of interest whether inflammatory biomarkers can improve dementia prediction models, such as the widely used Cardiovascular Risk Factors, Aging and Dementia (CAIDE) model.

methodsThe Olink Target 96 Inflammation panel was assessed in a nested case-cohort design within a large, population-based German cohort study (n = 9940; age-range: 50-75 years). All study participants who developed dementia over 20 years of follow-up and had complete CAIDE variable data (n = 562, including 173 Alzheimer's disease (AD) and 199 vascular dementia (VD) cases) as well as n = 1,356 controls were selected for measurements. 69 inflammation-related biomarkers were eligible for use. LASSO logistic regression and bootstrapping were utilized to select relevant biomarkers and determine areas under the curve (AUCs).

resultsThe CAIDE model 2 (including Apolipoprotein E (APOE) ε4 carrier status) predicted all-cause dementia, AD, and VD better than CAIDE model 1 (without APOE ε4) with AUCs of 0.725, 0.752 and 0.707, respectively. Although 20, 7, and 4 inflammation-related biomarkers were selected by LASSO regression to improve CAIDE model 2, the AUCs did not increase markedly. CAIDE models 1 and 2 generally performed better in mid-life (50-64 years) than in late-life (65-75 years) sub-samples of our cohort, but again, inflammation-related biomarkers did not improve their predictive abilities.

conclusionsDespite a lack of improvement in dementia risk prediction, the selected inflammation-related biomarkers were significantly associated with dementia outcomes and may serve as a starting point to further elucidate the pathogenesis of dementia.

Indexed as

Alzheimer’s diseaseCohort studyDementiaInflammationRisk predictionVascular dementia

Identifiers

PMID38570813
PMCPMC10988812
OpenAlexW4393864351

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.