DNA methylation age acceleration mediates the relationship between systemic inflammation and cognitive impairment

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F25%3A10507272" target="_blank" >RIV/00216208:11130/25:10507272 - isvavai.cz</a>

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=86aMtGFQE5" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=86aMtGFQE5</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1080/17501911.2025.2595905" target="_blank" >10.1080/17501911.2025.2595905</a>

Jazyk výsledku

angličtina

Název v původním jazyce

DNA methylation age acceleration mediates the relationship between systemic inflammation and cognitive impairment

Popis výsledku v původním jazyce

BACKGROUND: Chronic inflammation and DNA methylation are potential mechanisms in dementia etiology. The linkage between inflammation and DNA methylation age acceleration in shaping dementia risk remains understudied. We explored the association of inflammatory cytokines with cognitive impairment and whether DNA methylation age acceleration mediates this relationship. RESEARCH DESIGN AND METHODS: Using data from the 2016 Health and Retirement Study (n = 3,346, age &gt;50), we estimate the associations between each inflammatory cytokine (interleukin-6 (IL-6), C-reactive protein (CRP), and insulin-like growth factor-1 (IGF-1)), and cognitive status, classified using the Langa-Weir method. We tested if DNA methylation age acceleration mediated the relationship between systemic inflammation and cognitive impairment, adjusting for sociodemographic, behavioral factors, chronic conditions, and cell-type proportions. RESULTS: Cognitive impairment prevalence was 16%. A doubling of IL-6 was associated with a 12% higher odds of cognitive impairment (OR = 1.12, 95% CI: 1.02-1.22), and 0.77 years of GrimAge acceleration (95% CI: 0.64-0.90). Similar associations were found for CRP and IGF-1. Mediation analysis indicated that 17.7% (95% CI: 7.0-50.9%) of the IL-6-cognitive impairment association was mediated by the GrimAge acceleration. Comparable mediated estimates were found for CRP and IGF-1. CONCLUSIONS: Systemic inflammation is associated with cognitive impairment, with suggestive evidence that this relationship is partially mediated through DNA methylation age acceleration.

Název v anglickém jazyce

DNA methylation age acceleration mediates the relationship between systemic inflammation and cognitive impairment

Popis výsledku anglicky

BACKGROUND: Chronic inflammation and DNA methylation are potential mechanisms in dementia etiology. The linkage between inflammation and DNA methylation age acceleration in shaping dementia risk remains understudied. We explored the association of inflammatory cytokines with cognitive impairment and whether DNA methylation age acceleration mediates this relationship. RESEARCH DESIGN AND METHODS: Using data from the 2016 Health and Retirement Study (n = 3,346, age &gt;50), we estimate the associations between each inflammatory cytokine (interleukin-6 (IL-6), C-reactive protein (CRP), and insulin-like growth factor-1 (IGF-1)), and cognitive status, classified using the Langa-Weir method. We tested if DNA methylation age acceleration mediated the relationship between systemic inflammation and cognitive impairment, adjusting for sociodemographic, behavioral factors, chronic conditions, and cell-type proportions. RESULTS: Cognitive impairment prevalence was 16%. A doubling of IL-6 was associated with a 12% higher odds of cognitive impairment (OR = 1.12, 95% CI: 1.02-1.22), and 0.77 years of GrimAge acceleration (95% CI: 0.64-0.90). Similar associations were found for CRP and IGF-1. Mediation analysis indicated that 17.7% (95% CI: 7.0-50.9%) of the IL-6-cognitive impairment association was mediated by the GrimAge acceleration. Comparable mediated estimates were found for CRP and IGF-1. CONCLUSIONS: Systemic inflammation is associated with cognitive impairment, with suggestive evidence that this relationship is partially mediated through DNA methylation age acceleration.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30304 - Public and environmental health

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Epigenomics

ISSN

1750-1911

e-ISSN

1750-192X

Svazek periodika

17

Číslo periodika v rámci svazku

18

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

11

Strana od-do

1399-1409

Kód UT WoS článku

001633699300001

EID výsledku v databázi Scopus

2-s2.0-105024846093