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. Examples include Lesch-Nyhan syndrome and other neurological disorders, gout, Dalmatian hyperuricemic syndrome, and atherosclerosis. Several studies have suggested a causal role of UA in the neurodegenerative diseases. The possible neuroprotective role of UA has been shown by its anti-oxidative action of the non-crystal form of UA because; oxidative stress plays a critical role in neurodegeneration including dopaminergic degeneration in PD.
Case Report: Neurological Disorders
Case Report: Neurological Disorders
Case Report: Neurological Disorders
Case Report: Neurological Disorders
Case Report: Neurological Disorders
Case Report: Neurological Disorders
Editorial: Neurological Disorders
Editorial: Neurological Disorders
Short Communication: Neurological Disorders
Short Communication: Neurological Disorders
Posters & Accepted Abstracts: Neurological Disorders
Posters & Accepted Abstracts: Neurological Disorders
Posters: Neurological Disorders
Posters: Neurological Disorders
Posters & Accepted Abstracts: Neurological Disorders
Posters & Accepted Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Scientific Tracks Abstracts: Neurological Disorders
Posters & Accepted Abstracts: Journal of Pediatric Neurology and Medicine
Posters & Accepted Abstracts: Journal of Pediatric Neurology and Medicine
Neurological Disorders received 1343 citations as per Google Scholar report
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