Uric Acid (UA), historically considered as a waste of cellular metabolism, has now received increasing attention because it was found to directly participate in the pathogenesis of many human diseases including neurological disorders. On one hand, low levels of UA are detrimental to the neurons because of its induction it impairs antioxidant capacity in the cell. High levels of UA, on the other hand, lead to an inflammatory response contributing to gout or neuroprotection. Uric acid (UA) is a particularly interesting molecule that may be involved in the pathogenesis of AD, HD, PD, and MS AD is the most common cause of dementia affecting estimated 24 million people worldwide due to loss of neurons and synapses in the cerebral cortical and certain subcortical regions. More recent studies highlight the pathogenic property of UA that induces an inflammatory response contributing to gout and possibly UA-related CNS inflammatory diseases. Blocking antibodies against CD16 and CD11b selectively inhibit the activation of neutrophils and monocytes induced by MSU indicating CD16+ and CD11b+ cells as important mediators in MSU-induced inflammation. Since MSU is a direct and potent inflammasome activator, it is conceivable to speculate that high levels of UA may induce CNS inflammation and contribute to neurological disorders as well. Although hypouricemia has been associated with several neurological diseases, it has also been found that high levels of UA.
Last date updated on June, 2014