Figure 2.

Mechanism potentially involved in the pathophysiology of cognitive dysfunction related to uric acid metabolism. Local and systemic inflammation and oxidative stress, induced by xanthine oxidase activity and monosodium urate deposition in joints and arteries, represent an important indirect mechanism linking uric acid metabolism, serum uric acid abundance, and cognitive dysfunction, both of vascular and non-vascular origin. Dash and red arrows represent a direct product of uric acid and its production process. Continuous black arrows indicate the secondary effect of uric acid and its production. ROS: Reactive Oxygen Species; MSU: Monosodium Urate; H₂O₂: Hydrogen Peroxide; O₂⁻: Superoxide Anion; XO: Xanthine Oxidase; XDH: Xanthine Dehydrogenase; FAD: Flavin Adenine Dinucleotide; NO: Nitric Oxide: NADH: Nicotinamide Adenine Dinucleotide.