Abstract
BackgroundDespite known associations of lower serum uric acid (UA) with Alzheimer’s disease (AD) dementia or AD-related cognitive impairment, little is known regarding the underlying patho-mechanisms. We aimed to examine the relationships of serum UA with in vivo AD pathologies including cerebral beta-amyloid (Aβ) and tau deposition, AD-signature region cerebral glucose metabolism (AD-CM), and white matter hyperintensities (WMH). We also investigated the association between serum UA and cognitive performance, and then assessed whether such an association is mediated by the brain pathologies.MethodsA total of 430 non-demented older adults underwent comprehensive clinical assessments, measurement of serum UA level, and multimodal brain imaging, including Pittsburgh compound B-positron emission tomography (PET), AV-1451 PET, fluorodeoxyglucose (FDG)-PET, and magnetic resonance imaging scans. Mini-Mental State Examination (MMSE) and word list recall (WLR) test scores were used to measure cognitive performance.ResultsSerum UA level was significantly associated with AD-CM, but not with Aβ deposition, tau deposition, or WMH volume. Serum UA levels also had significant association with WLR and marginal association with MMSE; such associations disappeared when AD-CM was controlled as a covariate, indicating that AD-CM has a mediating effect.ConclusionThe findings of the present study indicate that there is an association of low serum UA with AD-related cerebral hypometabolism, and whether this represents a causal relationship remains to be determined.
Highlights
Uric acid (UA) is a naturally produced water-soluble antioxidant, which contributes more than half of the free radical scavenging activity in the peripheral nervous system (Ames et al, 1981; Choi et al, 2005; Gao et al, 2008)
Demographic and clinical characteristics of the participants are presented in Table 1; of the total 429 participants, 143 individuals had low serum UA levels, 140 had middle UA serum levels, and 146 had high serum UA levels
Serum UA was not associated with white matter hyperintensities (WMH)
Summary
Uric acid (UA) is a naturally produced water-soluble antioxidant, which contributes more than half of the free radical scavenging activity in the peripheral nervous system (Ames et al, 1981; Choi et al, 2005; Gao et al, 2008). Several studies showed that lower serum UA was associated with a markedly higher risk of progressing to AD dementia from a non-demented state (Rinaldi et al, 2003; Euser et al, 2009; Irizarry et al, 2009; Du et al, 2016). Despite such associations of lower serum UA with AD dementia or AD-related cognitive impairment, little is known regarding the underlying patho-mechanisms. Despite known associations of lower serum uric acid (UA) with Alzheimer’s disease (AD) dementia or AD-related cognitive impairment, little is known regarding the underlying patho-mechanisms. We investigated the association between serum UA and cognitive performance, and assessed whether such an association is mediated by the brain pathologies
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