Schretlen DJ, Inscore AB, Vannorsdall TD et al. Neurology 2007; 69:1418-1423.
The authors make the case for uric acid in brain function/dysfunction. UA is a natural antioxidant, with concentrations tenfold those of Vitamins c and e. Low UA is found in patients with MCI AD and PD. High UA predicts better outcome after stroke in one study (see Chamorro, Stroke, 2002) and in experimental models. However high UA also predicts occurrence of stroke, second stroke, fatal MI. Allopurinol protects against stroke damage in an animal model, and high UA correlates with HTN, atherosclerosis, type 2 DM and the metabolic syndrome. Studies show elderly participants with higher UA levels were 2.7 to 5.9 times more likely to be in the lowest quartile of processing speed, verbal and working memory.
In the present study, patients with higher UA were more likely to have increased volume of WMHs on brain MRI. There was a 4-5 x increased likelihood if having excessive ischemic burden.
The authors speculate that UA can be prooxidant as well as anti-oxidant.
This blogger, a skeptic, believes that high UA is a marker for dehydration and capillary sludging and that hydrating the elderly is a good way to reduce stroke. Therefore, aside from its biologic properties, UA is just a marker for the state of hydration. These authors from jhmi (johns hopkins) did not appreciate or address this obvious clinical point.
Postscript--review article Feig DI, Kang DH, Johnson RH NEJM 2008;359:1811-1821 "Uric acid and cardiovascular risk" also reviews subject from a different vantage point. They note Framingham does not currently consider urate a risk factor. This is a nice review article with lots of good references.
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