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Inflammatory Markers and their Relationship with Cognitive Function in Alzheimer’s Disease and Mild Cognitive Impairment. Systematic Review and Meta-Analysis

Maria Fernanda Serna; Mildrey Mosquera; Herney Andrés García-Perdomo
NeuroMolecular Medicine · Vol. 27, Issue 1 · 2025

Abstract

This study estimates the association between blood levels of inflammatory markers and cognitive function in adults with Alzheimer’s disease or mild cognitive impairment. A systematic review and meta-analysis were conducted to synthesize data from studies examining the relationship between blood levels of inflammatory markers and cognitive function in adults with Alzheimer’s disease or mild cognitive impairment. The search strategy was applied to the Medline database through MEDLINE (OVID), WEB OF SCIENCE, SCOPUS, LILACS, and the Cochrane Central Register of Controlled Trials (CENTRAL). Studies were selected based on predefined criteria. We included 84 studies in the qualitative synthesis, with 75 incorporated into the meta-analysis. In blood samples, subjects with Alzheimer’s disease showed significantly higher concentrations of IL-1β (mean difference 0.46 [95% CI: 0.35, 0.58]), IL-6 (3.41 [3.05, 3.78]), MCP-1 (26.20 [14.57, 37.82]), and TNF-α (6.68 [5.97, 7.39]), along with lower concentrations of IL-8 (− 1.46 [− 1.85, − 1.08]) and IL-10 (− 3.20 [− 4.21, − 2.20]). This systematic review and meta-analysis demonstrate significant alterations in inflammatory marker concentrations in blood samples of individuals with Alzheimer’s disease and mild cognitive impairment. Elevated levels of IL-1β, IL-6, MCP-1, and TNF-α, alongside reduced IL-8 and IL-10 levels, suggest a robust inflammatory response associated with Alzheimer’s disease.

Bibliographic Information

JournalNeuroMolecular Medicine
PublisherSpringer
Publication Date2025-07-25
Publication Year2025
Volume27
Issue1
Document TypeJournal Article
eISSN1559-1174
DOI10.1007/s12017-025-08866-w

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NARA Access Coverage2002-01-01~Current
Journal Homepagehttps://www.springer.com/journal/12017
Publisher PageOpen Publisher Page
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