The Role of Uric Acid and Methyl Derivatives in the Prevention of Age-Related Neurodegenerative Disorders

被引：45

作者：

Cutler, Roy G. ^{[1
]}

Camandola, Simonetta ^{[1
]}

Malott, Kelli F. ^{[1
]}

Edelhauser, Maria A. ^{[1
]}

Mattson, Mark P. ^{[1
,2
]}

机构：

[1] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA

[2] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

来源：

CURRENT TOPICS IN MEDICINAL CHEMISTRY | 2015年 / 15卷 / 21期

关键词：

Aging; Antioxidant; Caffeine; Neurodegeneration; Theobromine; Urate Oxidase; Uric acid; EXTRACELLULAR-SUPEROXIDE DISMUTASE; MILD COGNITIVE IMPAIRMENT; ISCHEMIC BRAIN-INJURY; PARKINSONS-DISEASE; MULTIPLE-SCLEROSIS; ALZHEIMERS-DISEASE; URATE OXIDASE; SERUM URATE; PLASMA ANTIOXIDANTS; HOMINOID EVOLUTION;

D O I：

10.2174/1568026615666150610143234

中图分类号：

R914 [药物化学];

学科分类号：

100705 [微生物与生化药学];

摘要：

High uric acid (UA) levels have been correlated with a reduced risk of many neurodegenerative diseases through mechanisms involving chelating Fenton reaction transitional metals, antioxidant quenching of superoxide and hydroxyl free radicals, and as an electron donor that increases antioxidant enzyme activity (e.g. SOD). However, the clinical usefulness of UA is limited by its' low water solubility and propensity to form inflammatory crystals at hyperuricemic levels. This review focuses on the role of UA in neuroprotection, as well as potential strategies aimed at increasing UA levels in the soluble range, and the potential therapeutic use of more water-soluble methyl-UA derivatives from the natural catabolic end-products of dietary caffeine, theophylline, and theobromine.

引用

页码：2233 / 2238

页数：6

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