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Cited by 56Dementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatments

Peripheral inflammatory biomarkers are associated with cognitive function and dementia: Framingham Heart Study Offspring cohort

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Chen, Jiachen, Doyle, Margaret F., Fang, Yuan, Mez, Jesse, Crane, Paul K., Scollard, Phoebe, ADSP Data Harmonization Consortium Cognitive Harmonization Core, Satizabal, Claudia L. +4 more·2023·Aging Cell
DOI 10.1111/acel.13955PMC PMC10577533
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Abstract

Inflammatory protein biomarkers induced by immune responses have been associated with cognitive decline and the pathogenesis of Alzheimer's disease (AD). Here, we investigate associations between a panel of inflammatory biomarkers and cognitive function and incident dementia outcomes in the well‐characterized Framingham Heart Study Offspring cohort. Participants aged ≥40 years and dementia‐free at Exam 7 who had a stored plasma sample were selected for profiling using the OLINK proteomics inflammation panel. Cross‐sectional associations of the biomarkers with cognitive domain scores (N = 708, 53% female, 22% apolipoprotein E (APOE) ε4 carriers, 15% APOE ε2 carriers, mean age 61) and incident all‐cause and AD dementia during up to 20 years of follow‐up were tested. APOE genotype‐stratified analyses were performed to explore effect modification. Higher levels of 12 and 3 proteins were associated with worse executive function and language domain factor scores, respectively. Several proteins were associated with more than one cognitive domain, including IL10, LIF‐R, TWEAK, CCL19, IL‐17C, MCP‐4, and TGF‐alpha. Stratified analyses suggested differential effects between APOE ε2 and ε4 carriers: most ε4 carrier associations were with executive function and memory domains, whereas most ε2 associations were with the visuospatial domain. Higher levels of TNFB and CDCP1 were associated with higher risks of incident all‐cause and AD dementia. Our study found that TWEAK concentration was associated both with cognitive function and risks for AD dementia. The association of these inflammatory biomarkers with cognitive function and incident dementia may contribute to the discovery of therapeutic interventions for the prevention and treatment of cognitive decline.

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  • In non-demented individuals, lipid, inflammatory, and metabolic profiles predict cognitive performance and its trajectory.

    “In non‐demented individuals, lipid, inflammatory, and metabolic profiles predict cognitive performance and its trajectory. 14 , 15”

    From Plasma extracellular vesicles from <i>APOE3</i> Christchurch carriers display a protective phenotype in early stages of autosomal dominant Alzheimer's disease (2026) · cites this paper as [15]

    The Abstract reports associations between inflammatory proteins and cognitive-domain scores in participants who were dementia-free at baseline. The Methods treat lipid and metabolic measures as covariates, not as profiles shown to predict cognition. The Discussion says the cognitive analyses were cross-sectional, so the paper does not establish prediction of cognitive trajectory. Page numbers are unavailable in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

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Chen, J., Doyle, M. F., Fang, Y., Mez, J., Crane, P. K., Scollard, P., ADSP Data Harmonization Consortium Cognitive Harmonization Core, Satizabal, C. L., Alosco, M. L., Qiu, W. Q., Murabito, J. M., & Lunetta, K. L.
Affiliations
  • Boston University (US)
  • University of Vermont (US)
  • University of Washington (US)
  • Department of Neurology Boston University Chobanian &amp; Avedisian School of Medicine Boston Massachusetts USA
Corresponding author
Lunetta, Kathryn L.
ORCID
Venue
Aging Cell
Publisher
Wiley
Published
2023-08-16
Volume
22
Issue
10
Pages
e13955-e13955
ISSN
  • 1474-9718 (ISSN-L)
  • 1474-9726
DOI
10.1111/acel.13955
PMC
PMC10577533
OpenAlex
W4385850958
Cited by
56
References
16
Citations by year
2026: 11 · 2025: 24 · 2024: 18 · 2023: 3
FWCI
11.47
Type
journal article
Language
en
Open access
Licence
Locations
  • Aging Cell (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
National Institutes of Health (R01AG067457)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
inflammatory markers, cognitive function, dementia, Alzheimer's disease, APOE ε4, APOE ε2, TWEAK, executive function, language, memory, lymphotoxin, CDCP1, IL-17C, CCL19, proteomics, cognitive decline
MeSH terms
Alzheimer Disease, Antigens, Neoplasm, Apolipoproteins E, Cognition, Cross-Sectional Studies, Female, Genotype, Humans, Longitudinal Studies, Male, Biomarkers, Cell Adhesion Molecules, Apolipoprotein E4, Apolipoprotein E2, Cognitive Dysfunction

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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