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KMID : 1100220110100020041
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Dementia and Neurocognitive Disorders
2011 Volume.10 No. 2 p.41 ~ p.46
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Uric Acid as a Compensator for Oxidative Stress in Alzheimer’s Disease
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Kim Sang-Dae
Yang Ji-Won
Youn Bang-Bu
Park Kee-Hyung
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Abstract
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Background: Uric acid (UA) is known to have neuroprotective effects by acting as a major plasma antioxidant. However, it is also known to be a pro-oxidant under certain circumstances. In this study, we analysed the association between UA and homocystein, which is a well-known pro-oxidant, as well as the association between UA and cognitive function in order to evaluate the neuroprotective function of UA in neurodegenerative disease progression.
Methods: Plasma UA and homocystein, along with the two other major plasma antioxidants albumin and bilirubin, were measured in 133 Alzhiemer’s disease (AD) patients, 98 Mild cognitive impairment (MCI) patients, and 77 normal elderly controls. The cognitive function of the subjects was evaluated by Mini Mental Status Examination (MMSE). By using linear regression analysis, we investigated the association between UA with homocystein in each of these groups. Furthermore, the association between UA levels and the MMSE score was also analyzed. All analyses were adjusted for age, sex, education, hypertension, and diabetes mellitus.
Results: Homocystein increased in MCI, AD group compared with the control group. In the AD group, there was a statistically significant increase of UA compared with the MCI group, after adjusting for age, gender, hypertension, diabetes mellitus, and education (p=0.017). Linear regression analysis showed that increasing homocystein predicted increasing UA in MCI and AD patients (β=1.12, SE=0.36, p=0.002; β=1.79, SE=0.43, p<0.001, respectively). Furthermore, increasing UA predicted increasing MMSE in AD patients (β=0.48, SE=0.21, p=0.02), but not in MCI patients when adjusted for confounders.
Conclusions: We suggest that UA might be related to neuroprotective compensation for oxidative stress which would reduce the rate of cognitive decline in AD patients.
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KEYWORD
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Alzheimer’s disease (AD), Mild cognitive impairment (MCI), Uric acid (UA), Oxidative stress, Neuroprotection, Cognitive function
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