Yu Zhange, Zhang Shuai, Wang Dongdong, Fan Meng, Gao Fuqiang, Sun Wei, Li Zirong, Li Shiliang
Department of Acupuncture, China-Japan Friendship Hospital, Beijing Department of Neurology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu Province Department of Orthopedics, Tumd Right Banner Hospital, Baotou City Department of Orthopedics, China-Japan Friendship Hospital, Beijing, China.
Medicine (Baltimore). 2017 Nov;96(45):e8502. doi: 10.1097/MD.0000000000008502.
Parkinson disease (PD) is a neurodegenerative disease characterized by chronic and progressive loss of dopaminergic neurons in substansia nigra pars compacta. Oxidative stress is proposed to play a critical role in the pathogenesis of PD. Uric acid (UA), as an important physiological antioxidant, is identified a molecular predictor associated with a decreased risk and a slower disease progression for PD and potential neuroprotectant of PD by increasing epidemiological and clinical evidences. Within this review, we will present a comprehensive overview of the data linking UA to PD in recent years.
We searched PubMed, EMBASE, Web of Science databases for relevant studies. Any observational or experimental studies that evaluated UA and PD were our goal of searching the electric databases.
Twelve studies that evaluated UA and PD were identified in this review. We reviewed the roles of UA in the pathogenesis of PD, the association of UA with morbidity, severity/progression, nonmotor symptoms, motor complications of PD, with an attempt to provide new ideas for diagnosis and treatment in PD.
Our findings supported that lots of clinical and epidemiological data observed lower UA levels in PD patients. Manipulation of UA or its precursors' concentration could be effective to treat or prevent PD. However, it is still suspectable that higher UA levels are better enough to PD patients. Furthermore, for the complex nature of PD and its heterogeneous genetic and environmental influences, it is inadequate for just manipulating UA in treating the disease.
帕金森病(PD)是一种神经退行性疾病,其特征是黑质致密部多巴胺能神经元慢性进行性丧失。氧化应激被认为在PD的发病机制中起关键作用。尿酸(UA)作为一种重要的生理性抗氧化剂,通过越来越多的流行病学和临床证据,被确定为与PD风险降低和疾病进展缓慢相关的分子预测指标以及PD的潜在神经保护剂。在本综述中,我们将全面概述近年来将UA与PD联系起来的数据。
我们在PubMed、EMBASE、科学网数据库中搜索相关研究。评估UA与PD的任何观察性或实验性研究都是我们搜索电子数据库的目标。
本综述中确定了12项评估UA与PD的研究。我们综述了UA在PD发病机制中的作用,UA与PD发病率、严重程度/进展、非运动症状、运动并发症的关联,试图为PD的诊断和治疗提供新思路。
我们的研究结果支持大量临床和流行病学数据观察到PD患者的UA水平较低。调节UA或其前体的浓度可能有效治疗或预防PD。然而,较高的UA水平对PD患者是否足够好仍值得怀疑。此外,由于PD的复杂性及其异质性的遗传和环境影响,仅通过调节UA来治疗该疾病是不够的。