Abstract
BackgroundSerum uric acid (UA) could exert neuro-protective effects against Alzheimer's disease (AD) via its antioxidant capacities. Many studies investigated serum UA levels in AD patients, but to date, results from these observational studies are conflicting.MethodsWe conducted a meta-analysis to compare serum UA levels between AD patients and healthy controls by the random-effects model. Studies were identified by searching PubMed, ISI Web of Science, EMBASE, and the Cochrane library databases from 1966 through July 2013 using the Medical Subject Headings and keywords without restriction in languages. Only case-control studies were included if they had data on serum UA levels in AD patients and healthy controls. Begg's funnel plot and Egger's regression test were applied to assess the potential publication bias. Sensitivity analyses and meta-regression were conducted to explore possible explanations for heterogeneity.ResultsA total of 11 studies met the inclusion criteria including 2708 participants were abstracted. Serum UA levels were not significantly different in AD patients compared to healthy controls (standardized mean difference (SMD) = −0.50; 95% confidence interval (CI): −1.23 to 0.22). Little evidence of publication bias was observed. Sensitivity analyses showed that the combined SMD was consistent every time omitting any one study, except only one study which greatly influenced the overall results. Meta-regression showed that year of publication, race, sample size, and mean age were not significant sources of heterogeneity.ConclusionOur meta-analysis of case-control studies suggests that serum UA levels do not differ significantly in AD patients, but there may be a trend toward decreased UA in AD after an appropriate interpretation. More well-designed investigations are needed to demonstrate the potential change of serum UA levels in AD patients.
Highlights
Alzheimer’s disease (AD) is the most common neurodegenerative dysfunction of the central nervous system, characterized by brain atrophy and accumulation of amyloid-plaques and neurofibrillary tangles throughout the cortex by the end of the disease [1]
Considering these inconsistent possibilities, we tried to establish what consensus could be reached from various studies by examining the change of serum uric acid (UA) levels in AD patients compared to healthy controls with meta-analytic techniques
Full-text evaluation were conducted in the remaining 21 articles, and 10 articles were excluded for not fulfilling our inclusion criteria: 3 articles reported insufficient data on serum UA levels; 3 articles did not apply wellaccepted diagnosis standard for AD; 2 articles used cerebrospinal fluid (CSF), not blood as specimen; 1 article was excluded due to no original data reported; 3 studies were based on the same population, the one containing the most complete and relevant data was used
Summary
Alzheimer’s disease (AD) is the most common neurodegenerative dysfunction of the central nervous system, characterized by brain atrophy and accumulation of amyloid-plaques and neurofibrillary tangles throughout the cortex by the end of the disease [1]. UA is an endogenously produced water-soluble antioxidant [29,30], accounting for up to 60% of the free radical scavenging capacity in the peripheral system by quenching superoxide and singlet oxygen [31,32] These qualities make UA an attractive CNS antioxidant, and its potential protective effects on AD have been reported in prior studies. Some studies suggest that patients with higher serum UA levels have a markedly lower risk of progressing from impaired cognitive function to dementia [37,38], while some studies found that even mild elevation of UA might enhance the risk of cognitive decline in older adults [39]. Many studies investigated serum UA levels in AD patients, but to date, results from these observational studies are conflicting
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