The association of serum uric acid with cognitive impairment and ATN biomarkers

BackgroundCognitive impairment (CI) has become a worldwide health problem. The relationship between CI and uric acid (UA) is contradictory.ObjectiveWe included participants with a full spectrum of CI, from cognitively unimpaired (CU) to dementia, from the Chongqing Ageing & Dementia Study (C...

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Main Authors: Shan Huang, Jun Wang, Dong-Yu Fan, Tong Luo, Yanli Li, Yun-Feng Tu, Ying-Ying Shen, Gui-Hua Zeng, Dong-Wan Chen, Ye-Ran Wang, Li-Yong Chen, Yan-Jiang Wang, Junhong Guo
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-07-01
Series:Frontiers in Aging Neuroscience
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Online Access:https://www.frontiersin.org/articles/10.3389/fnagi.2022.943380/full
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Summary:BackgroundCognitive impairment (CI) has become a worldwide health problem. The relationship between CI and uric acid (UA) is contradictory.ObjectiveWe included participants with a full spectrum of CI, from cognitively unimpaired (CU) to dementia, from the Chongqing Ageing & Dementia Study (CADS).MethodsFirst, we identified the relationships between serum UA (sUA) and cognitive function in different stages of CI. Second, we analyzed these relationships among different stages and types of CI. Finally, we explored the association between sUA and amyloid/tangle/neurodegeneration (ATN) biomarkers.ResultsWe recruited 427 participants from the CADS, including 382 participants with mini-mental state examination (MMSE) evaluation. The levels of sUA were positively correlated with MMSE scores (p < 0.001), and the correlation was prominent in the course of dementia and in the type of Alzheimer’s disease (AD). The levels of UA had a positive correlation with plasma amyloid-β 42 (Aβ42) (p = 0.004). Higher levels of sUA weakened the correlation of MMSE scores with CSF ATN biomarkers and the correlation of CSF Aβ42 with tau.ConclusionUA is positively correlated with cognitive function, especially in the advanced stage of AD. The probable neuroprotective effects of sUA mainly act on Aβ42 and the downstream pathological cascade.
ISSN:1663-4365