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All study participants who developed dementia over 20 years of follow-up and had complete CAIDE variable data (<jats:italic>n<\/jats:italic>\u2009=\u2009562, including 173 Alzheimer\u2019s disease (AD) and 199 vascular dementia (VD) cases) as well as<jats:italic>n<\/jats:italic>\u2009=\u20091,356 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).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The CAIDE model 2 (including Apolipoprotein E (<jats:italic>APOE<\/jats:italic>) \u03b54 carrier status) predicted all-cause dementia, AD, and VD better than CAIDE model 1 (without<jats:italic>APOE<\/jats:italic>\u03b54) 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\u201364 years) than in late-life (65\u201375 years) sub-samples of our cohort, but again, inflammation-related biomarkers did not improve their predictive abilities.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec>","DOI":"10.1186\/s12979-024-00427-2","type":"journal-article","created":{"date-parts":[[2024,4,3]],"date-time":"2024-04-03T07:02:16Z","timestamp":1712127736000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Addition of inflammation-related biomarkers to the CAIDE model for risk prediction of all-cause dementia, Alzheimer\u2019s disease and vascular dementia in a prospective study"],"prefix":"10.1186","volume":"21","author":[{"given":"Kira","family":"Trares","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manuel","family":"Wiesenfarth","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hannah","family":"Stocker","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Laura","family":"Perna","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Agnese","family":"Petrera","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefanie M.","family":"Hauck","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Konrad","family":"Beyreuther","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hermann","family":"Brenner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ben","family":"Sch\u00f6ttker","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2024,4,3]]},"reference":[{"key":"427_CR1","unstructured":"Prince M, Wimo A, Guerchet M, Ali G-C, Wu Y-T, Prina M. 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