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@ARTICLE{Trares:289223,
      author       = {K. Trares$^*$ and M. Wiesenfarth$^*$ and H. Stocker$^*$ and
                      L. Perna and A. Petrera and S. M. Hauck and K. Beyreuther
                      and H. Brenner$^*$ and B. Schöttker$^*$},
      title        = {{A}ddition of inflammation-related biomarkers to the
                      {CAIDE} model for risk prediction of all-cause dementia,
                      {A}lzheimer's disease and vascular dementia in a prospective
                      study.},
      journal      = {Immunity $\&$ ageing},
      volume       = {21},
      number       = {1},
      issn         = {1742-4933},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2024-00657},
      pages        = {23},
      year         = {2024},
      note         = {#EA:C070#LA:C070#},
      abstract     = {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.},
      keywords     = {Alzheimer’s disease (Other) / Cohort study (Other) /
                      Dementia (Other) / Inflammation (Other) / Risk prediction
                      (Other) / Vascular dementia (Other)},
      cin          = {C070 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38570813},
      doi          = {10.1186/s12979-024-00427-2},
      url          = {https://inrepo02.dkfz.de/record/289223},
}