Department of Geriatrics, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu City, Sichuan Province, China.
Biomed Res Int. 2021 Jun 2;2021:5525710. doi: 10.1155/2021/5525710. eCollection 2021.
As a powerful antioxidant in the human body, uric acid (UA) has been the subject of increasing research that focused on its influence on Alzheimer's disease (AD) in recent years. The latest literature was gathered to describe the influence of serum uric acid (SUA) level on the onset and progression of AD and to analyze the possibility that SUA is a biomarker of Alzheimer's disease. A large number of existing studies suggested that the SUA level was lower or tended to decrease in patients with AD, and increased SUA level may have a protective effect in AD, which could reduce the risk of onset and slowing the course of the disease. However, some Mendelian randomization analyses suggested that genetically determined uric acid was not associated with AD risk. Existing research results are contradictory due to the high inconsistency of the studies, the selection of subjects, and other factors. UA also showed a strong association with cognitive function, and there appeared to be a gender-selective neuroprotective action. Due to its potent antioxidant properties, the low uric acid level may contribute to oxidative stress to accelerate disease progression. But some preclinical data showed a possibility that in some special cases, UA had a prooxidant properties. The possibility was raised in the discussion of the underlying mechanism that both the low uric acid level and the rapidly progressive course of the disease were the consequence of malnutrition. This paper reviews recent advances in the study of SUA and AD which offers the possibility of new biomarker, new prevention, and treatment strategies for Alzheimer's disease.
尿酸作为人体内一种强大的抗氧化剂,近年来其对阿尔茨海默病(AD)的影响一直是研究的热点。本研究旨在综述血清尿酸(SUA)水平对 AD 发病和进展的影响,并分析 SUA 作为 AD 生物标志物的可能性。大量现有研究表明,AD 患者的 SUA 水平较低或呈下降趋势,而升高的 SUA 水平可能对 AD 具有保护作用,降低发病风险并减缓疾病进程。然而,一些孟德尔随机分析表明,遗传决定的尿酸与 AD 风险无关。由于研究间的高度不一致、研究对象的选择等因素,现有的研究结果存在矛盾。UA 与认知功能也有很强的相关性,并且似乎存在性别选择性的神经保护作用。由于其强大的抗氧化特性,低尿酸水平可能导致氧化应激加速疾病进展。但一些临床前数据表明,在某些特殊情况下,UA 可能具有促氧化剂特性。在讨论潜在机制时提出了这种可能性,即低尿酸水平和疾病的快速进展过程都是营养不良的结果。本文综述了 SUA 与 AD 研究的最新进展,为 AD 的新生物标志物、新的预防和治疗策略提供了可能。