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High Levels of Uric Acid May Cause Cerebral Strokes, Affecting Cognitive Function: Presented at ANA

By Jacquelyn Beals

WASHINGTON, DC -- October 17, 2007 -- High levels of serum uric acid (UA) in the elderly may cause cerebral strokes that lead to cognitive dysfunction, according to researchers presenting their findings here at the Annual Meeting of the American Neurological Association (ANA). This finding suggests that reducing serum UA might decrease the occurrence of cognitive dysfunction.

"Even minimal elevations in serum UA are associated with structural and functional brain changes, specifically involving the development of ischaemic injury," noted lead author Tracy D. Vannorsdall, PhD, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.

In this cross-sectional, observational study, 180 adults were enrolled from the Johns Hopkins Aging, Brain Imaging, and Cognition Study. Participant ages ranged from 20 to 96. All completed neuropsychological testing to assess cognitive abilities, and clinical tests including non-fasting blood samples for serum UA.

In normal, healthy adults, cerebral ischaemia is often indicated by hyperintensities in the cerebral white matter, detected by magnetic resonance imaging (MRI). These white matter hyperintensities (WMH) are increasingly common in "advancing age, cerebral atrophy, cerebrovascular risk factors such as hypertension and stroke, dementia, and cognitive dysfunction in the non-demented," the authors noted. In this study, images from brain MRI were used to calculate the "WMH burden" -- the ratio between the WMH volume and total brain volume.

Data analysis established that higher serum UA levels were associated with greater WMH burden (r =.232; P =.002); they were also associated with lower scores in 4 of the 8 areas of cognitive functioning. Greater WMH burden was associated with lower performance in 7 of the 8 areas of cognitive functioning (P values <.05). These results indicate an association between higher serum UA levels and lower cognitive performance.

The researchers add, however, that "once a term for WMH volume was added to the regression models, the UA-cognition associations were attenuated." In this latter analysis, the levels of UA were no longer predictive of cognitive dysfunction. Further analysis also determined that the previously detected association between verbal learning/memory and WMH burden no longer existed once serum UA levels were included in the model.

The inhibitory interaction of UA with nitric oxide (which mediates vascular tone) and the decreased capacity for vasodilatation in the cortex of patients with WMH both support impaired vascular tone as a possible mechanism for UA influence on cortical function.

Future clinical trials could determine whether medications that reduce production of serum UA, even within normal levels, would also decrease the occurrence of cerebral ischaemia and related cognitive dysfunction.

Individuals with high levels of serum UA are at a lower risk for Parkinson's disease, while those with low levels of serum UA are more likely to develop Alzheimer's disease. This apparent neuroprotective role of UA is complicated by the observation that high serum UA is common in many diseases, including stroke, diabetes, and hypertension.


[Presentation title: Cerebral Ischemia Mediates the Serum Uric Acid & Cognition Association. Abstract 25]

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