TY  - JOUR
AB  - BACKGROUND: 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. METHODS: 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). RESULTS: 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. CONCLUSIONS: 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.
AU  - Trares, K.*
AU  - Wiesenfarth, M.*
AU  - Stocker, H.*
AU  - Perna, L.*
AU  - Petrera, A.
AU  - Hauck, S.M.
AU  - Beyreuther, K.*
AU  - Brenner, H.*
AU  - Schöttker, B.*
C1  - 70438
C2  - 55628
CY  - Campus, 4 Crinan St, London N1 9xw, England
TI  - 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.
JO  - Immun. Ageing
VL  - 21
IS  - 1
PB  - Bmc
PY  - 2024
SN  - 1742-4933
ER  - 

TY  - JOUR
AB  - Background: Obesity is associated with chronic low-grade inflammation, which is underpinned by the presence of elevated levels of circulating proinflammatory cytokines in obese individuals. Due to the close relationship between adipose tissue and the immune system, it can be speculated that the accumulation of fat may influence the frequency and phenotype of lymphocyte populations. The aim of our study was to investigate whether body fat distribution is associated with B lymphocyte composition in peripheral blood. We examined the association between visceral (VAT) and total body fat (TBF) and the frequencies of B-cell subsets in 238 subjects over a period of up to one year using random intercept models. B lymphocyte subsets were determined by fluorescence-based flow cytometry. Results: Inverse associations were found between body fat measurements and plasma blasts, memory B cells, and IgM −IgD− cells. VAT, but not TBF, was positively associated with naive CD19 cells. In our analyses, both VAT and TBF showed positive associations with IgD only B cells. Conclusions: In conclusion, body fat accumulation seems to be associated with a lower proportion of antibody-secreting plasma blasts and memory cells and an increasing amount of partially anergic, naive CD19 cells.
AU  - Prechtl, P.*
AU  - Schmitz, T.*
AU  - Pochert, N.
AU  - Traidl-Hoffmann, C.
AU  - Linseisen, J.*
AU  - Meisinger, C.*
AU  - Freuer, D.*
C1  - 68284
C2  - 54705
TI  - Association between body fat distribution and B-lymphocyte subsets in peripheral blood.
JO  - Immun. Ageing
VL  - 20
IS  - 1
PY  - 2023
SN  - 1742-4933
ER  -