Serum Uric Acid Levels in Neurodegenerative Disorders: A Cross-Sectional Study

被引:7
|
作者
Aerqin, Qiaolifan [1 ,2 ,3 ]
Jia, Sha-Sha [4 ]
Shen, Xue-Ning [1 ,2 ,3 ]
Li, Quan [5 ]
Chen, Ke-Liang [1 ,2 ,3 ]
Ou, Ya-Nan [6 ]
Huang, Yu-Yuan [1 ,2 ,3 ]
Dong, Qiang [1 ,2 ,3 ]
Chen, Shu-Fen [1 ,2 ,3 ]
Yu, Jin-Tai [1 ,2 ,3 ]
机构
[1] Fudan Univ, Huashan Hosp, State Key Lab Med Neurobiol, Dept Neurol, Shanghai 200040, Peoples R China
[2] Fudan Univ, Huashan Hosp, State Key Lab Med Neurobiol, Inst Neurol, Shanghai 200040, Peoples R China
[3] Fudan Univ, MOE Frontiers Ctr Brain Sci, Shanghai Med Coll, Shanghai 200040, Peoples R China
[4] Nanjing Med Univ, Changzhou Peoples Hosp 2, Dept Neurol, Changzhou, Jiangsu, Peoples R China
[5] Fudan Univ, Shanghai Med Coll, Huashan Hosp, Dept Lab Med,Hongqiao Branch, Shanghai, Peoples R China
[6] Qingdao Univ, Qingdao Municipal Hosp, Dept Neurol, Qingdao, Peoples R China
基金
中国国家自然科学基金;
关键词
Cognition; neurodegeneration; oxidative stress; uric acid; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; DIAGNOSTIC-CRITERIA; CEREBROSPINAL-FLUID; PLASMA URATE; FOLLOW-UP; RISK; DEMENTIA; ASSOCIATION; PROGRESSION;
D O I
10.3233/JAD-220432
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: Excessive oxidative stress may contribute to neurodegeneration by leading to protein aggregation and mitochondrial dysfunction. Uric acid (UA) is an important endogenous antioxidant that protects against oxidative stress, yet its exact role in neurodegeneration remains unclear. Objective: To explore the performance of serum UA in neurodegenerative disorders. Methods: A total of 839 controls and 840 patients, including Alzheimer's disease (AD), Parkinson's disease (PD), multiple system atrophy (MSA), progressive supranuclear palsy (PSP), frontotemporal dementia (FTD), dementia with Lewy bodies (DLB), motor neuron disease (MND), Creutzfeldt-Jakob disease (CJD), and mixed dementia (MixD) were enrolled. Fasting serum UA levels were measured in all participants and compared between patients and controls. Linear regression models were utilized to explore possible relationships of serum UA with cognition, disease duration, age, and age of onset. Results: Compared to controls (355.48 +/- 85.38 mu mol/L), serum UA was significantly lower in AD (291.29 +/- 83.49 mu mol/L, p < 0.001), PD (286.95 +/- 81.78 mu mol/L, p < 0.001), PSP (313.32 +/- 88.19 mu mol/L, p < 0.001), FTD (313.89 +/- 71.18 mu mol/L, p = 0.001), and DLB (279.23 +/- 65.51 mu mol/L, p < 0.001), adjusting for confounding factors including age, gender, education, etc. In addition, serum UA was positively correlated with cognitive levels in all patients (Mini-Mental State Examination: r = 0.136, p = 0.001; and Montreal Cognitive Assessment Scale: r = 0.108, p = 0.009). Conclusion: Decreased levels of serum UA were correlated with AD, PD, PSP, FTD, and DLB, offering significant potential as a promisingly relevant, less-invasive marker of multiple neurodegenerative disorders.
引用
收藏
页码:761 / 773
页数:13
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