PubMed article abstract display

Abstract

Objective: Mild cognitive impairment (MCI) is a common, chronic, and complex disease in the elderly, which is often influenced by a variety of factors that include nutrition and inflammation. This study was undertaken to evaluate the mediation effects of inflammation on the association between vitamin D levels and MCI.

Methods: We explored the associations of inflammation and cognitive impairment related to 25(OH)D₃ deficiency among 360 older people from the communities in China. Demographic characteristics, lifestyle, and health status were investigated by questionnaire, cognitive function was detected by MoCA, and plasma 25(OH)D₃, interleukin-1β (IL-1β), and interleukin-18 (IL-18) were measured by ELISA. Spearman's correlation analysis and logistic regression analysis were used to analyze the relationship among 25(OH)D₃, IL-1β, and IL-18 in the MCI group and the control group and further to analyze the relationship between 25(OH)D₃ and inflammatory factors in the MCI group. Finally, mediation analysis was performed to evaluate whether inflammation mediated the effect of 25(OH)D₃ deficiency on cognitive impairment.

Results: There were lower plasma 25(OH)D₃ concentration and higher IL-1β and IL-18 levels in the MCI group compared with the controls. The levels of 25(OH)D₃ were positively correlated with the MoCA scores and scores of different domains; the levels of IL-1β and IL-18 were negatively correlated with them (p < 0.05). In multivariate logistic analysis, there were significant associations among 25(OH)D₃, IL-1β, IL-18, and MCI after adjusted. Further analysis revealed the significant association between the subjects with VD deficiency and the highest quartile of IL-18 in MCI (OR = 4.066), not with IL-1β after adjusting the confounding variables in MCI group. Ultimately, mediation analysis suggested that IL-1β and IL-18 could explain 25.4 and 17.5% of effect of the risk of cognitive impairment related to 25(OH)D₃ deficiency.

Conclusion: Our findings suggested that 25(OH)D₃ deficiency could increase the risk of cognitive impairment by a mechanism partly involving inflammation. Therefore, vitamin D supplementation may improve or delay the decline in cognitive function caused by inflammation in the elderly.

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