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Original Article
Dementia and Neurocognitive Disorders 2011: 10: 2: 41-46

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알츠하이머병 환자에서 산화적 스트레스에 대한 요산의 보상적 역할
김상대*·양지원†·윤방부‡박기형†
홍성군보건소*, 가천의대 길병원 신경과학교실†, 가천의대 뇌건강센터‡
Uric Acid as a Compensator for Oxidative Stress in Alzheimer’s Disease
Sang-Dae Kim, M.D.*, Ji-Won Yang, M.D.†, Bang Bu Youn,M.D., Ph.D.‡, Kee Hyung Park, M.D., Ph.D.†
Public Health Center*, Hongseong; Department of Neurology†, Gachon University, Gil Medical Center, Incheon; The Gachon Brain Health Center‡, Gachon University, Gil Medical Center, Incheon, Korea
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.
Key Words: Alzheimer’s disease (AD), Mild cognitive impairment (MCI), Uric acid (UA), Oxidative stress, Neuroprotection, Cognitive function