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Polyphenol intake beneficially associates with inflammation and cognitive performance, and is mediated by MRI‐derived features

认知功能衰退 认知 医学 炎症 睡眠剥夺对认知功能的影响 多酚 痴呆 全身炎症 生物标志物 神经退行性变 内科学 生理学 疾病 抗氧化剂 生物 生物化学 精神科
作者
Elliot R Dryer‐Beers,Paul M. Matthews,Gary Frost,Jennifer Griffin
出处
期刊:Alzheimers & Dementia [Wiley]
卷期号:19 (S23)
标识
DOI:10.1002/alz.079646
摘要

Abstract Background Early changes to cognitive performance and neurophysiological biomarkers offer insights into one’s future risk of developing Alzheimer’s disease or other dementias. Evidence suggests a link between polyphenol intake and reduced incidence of age‐associated cognitive decline and neurodegeneration. These relationships may be driven by the effect of dietary polyphenols on inflammation and degeneration of critical neurological structures and systems. These relationships are challenging to assess, as few cohorts allow cohesive assessment of polyphenol intake, systemic inflammation, neurophysiological measures and cognition. Method Polyphenol intake was assessed in two UK cohorts: The Airwave Health Monitoring Study and UK Biobank (UKB). Diet diary and questionnaire data were integrated with polyphenol composition data from Phenol‐Explorer to allow for testing of associations between polyphenol intake, blood biomarkers of inflammation, and cognitive performance. 9008 Airwave participants and 209,163 UKB participants were included in a cross‐sectional analysis. C‐reactive protein (CRP) and fibrinogen were used as blood biomarkers of inflammation, and cognitive assessments included reaction time (milliseconds) and fluid intelligence (score /13). Neuroimaging assessments included grey matter volumes and white matter integrity, and were considered individually and using PCA. Result Linear regressions showed inverse associations between total polyphenol intake and CRP: β ‐0.00702 (Airwave) and β = ‐0.00672 (UKB), both P <0.001, as well as fibrinogen: β ‐0.00221; P = 0.038 (Airwave only), in addition to biomarker associations with polyphenols at the compound group level. Regarding cognition, linear regressions revealed beneficial associations between total intake and performance in fluid intelligence tests: β 0.00657; P = 0.009 (Airwave) and β 0.00715, P <0.001 (UKB), and reaction time β ‐0.0000977; P = 0.020 (UKB). Mediations of the polyphenol‐fluid intelligence relationship were detected for IDPs including grey matter volumes of hippocampal‐associated regions, and white matter integrity measured using ISOVF. Conclusion We described polyphenol intake in two large, contemporary UK cohorts, and discovered associations between higher intake and improved inflammatory markers and cognitive performance, as well as mediations of the polyphenol‐cognition relationship by physical neurological markers. This contributes to evidence supporting the health benefits of dietary polyphenols, clarifies the physiological pathways through which they may act, and highlights their relevance when considering preventative interventions for neurodegeneration.
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