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

Article type: Research Article

Authors: Aerqin, Qiaolifan^a | Jia, Sha-Sha^b | Shen, Xue-Ning^a | Li, Quan^c | Chen, Ke-Liang^a | Ou, Ya-Nan^d | Huang, Yu-Yuan^a | Dong, Qiang^a | Chen, Shu-Fen^{a; *} | Yu, Jin-Tai^{a; *}

Affiliations: [a] Department of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China | [b] Department of Neurology, Changzhou Second People’s Hospital, Nanjing Medical University, Changzhou, China | [c] Department of Laboratory Medicine, Huashan Hospital Hongqiao Branch, Shanghai Medical College, Fudan University, Shanghai, China | [d] Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China

Correspondence: [*] Correspondence to: Prof. Jin-Tai Yu, MD, PhD and Shu-Fen Chen, MD, PhD, Department of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200040, China. Tel.: +86 21 52888163; Fax: +86 21 62483421; E-mails:jintai_yu@fudan.edu.cn (Jin-Tai Yu), chenshufen@fudan.edu.cn (Shu-Fen Chen).

Abstract: 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 μmol/L), serum UA was significantly lower in AD (291.29 ± 83.49 μmol/L, p < 0.001), PD (286.95 ± 81.78 μmol/L, p < 0.001), PSP (313.32 ± 88.19 μmol/L, p < 0.001), FTD (313.89 ± 71.18 μmol/L, p = 0.001), and DLB (279.23 ± 65.51 μmol/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.

Keywords: Cognition, neurodegeneration, oxidative stress, uric acid

DOI: 10.3233/JAD-220432

Journal: Journal of Alzheimer's Disease, vol. 90, no. 2, pp. 761-773, 2022