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.
Keywords: Aging, Antioxidant, Caffeine, Neurodegeneration, Theobromine, Urate Oxidase, Uric acid.
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