ArticleBMC geriatrics2026
Does resolvin D2 reflect cognitive impairment in older adults? A clinical and biomarker analysis.
Article in BMC geriatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAlzheimer's disease is a progressive neurodegenerative disorder with an unclear etiology, in which inflammation and impaired resolution pathways may play a role. This study investigated the relationship between serum Resolvin D2 levels and cognitive status in individuals with normal cognition, mild cognitive impairment, and Alzheimer's disease.
methodsIn this cross-sectional study, 165 adults aged ≥ 65 years who attended a tertiary geriatric clinic between 2022 and 2025 were classified as cognitively normal, mild cognitive impairment, or Alzheimer's disease. Demographic, clinical, laboratory, and comprehensive geriatric assessment data were collected. Serum Resolvin D2 levels were measured using ELISA and analyzed in relation to cognitive status. Logistic regression and ROC curve analyses were performed to evaluate the potential diagnostic value of Resolvin D2.
resultsResolvin D2 levels did not differ significantly among cognitive status groups. In multivariate analyses, Resolvin D2 was not an independent predictor of dementia or cognitive impairment. ROC curve analyses demonstrated limited diagnostic performance of Resolvin D2 compared with established clinical and laboratory indicators. These findings suggest that serum Resolvin D2 levels may have limited utility as a standalone biomarker, although their role within neuroinflammatory and resolution pathways warrants further investigation.
conclusionSerum Resolvin D2 levels have limited ability to distinguish older adults with cognitive impairment or dementia from cognitively normal individuals. In contrast, S-MMSE, Lawton IADL scores, and comorbidity burden remain independent predictors of cognitive status. While Resolvin D2 shows anti-inflammatory and pro-resolving effects in experimental models, its value as a standalone biomarker for cognitive decline appears limited. Larger, prospective, multi-biomarker studies are needed to clarify its role.
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