%0 Journal Article
%A Trares, Kira
%A Wiesenfarth, Manuel
%A Stocker, Hannah
%A Perna, Laura
%A Petrera, Agnese
%A Hauck, Stefanie M
%A Beyreuther, Konrad
%A Brenner, Hermann
%A Schöttker, Ben
%T 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.
%J Immunity & ageing
%V 21
%N 1
%@ 1742-4933
%C London
%I BioMed Central
%M DKFZ-2024-00657
%P 23
%D 2024
%Z #EA:C070#LA:C070#
%X It is of interest whether inflammatory biomarkers can improve dementia prediction models, such as the widely used Cardiovascular Risk Factors, Aging and Dementia (CAIDE) model.The 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).The 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.Despite 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.
%K Alzheimer’s disease (Other)
%K Cohort study (Other)
%K Dementia (Other)
%K Inflammation (Other)
%K Risk prediction (Other)
%K Vascular dementia (Other)
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:38570813
%R 10.1186/s12979-024-00427-2
%U https://inrepo02.dkfz.de/record/289223