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Background: 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 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. Methods: A 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. Results: Serum 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. Conclusion: The 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.

Background An emerging body of literature has indicated that moderate alcohol intake may be protective against Alzheimer disease (AD) dementia. However, little information is available regarding whether moderate alcohol intake is related to reductions in amyloid-beta (Aβ) deposition, or is protective via amyloid-independent mechanisms in the living human brain. Here we examined the associations of moderate alcohol intake with in vivo AD pathologies, including cerebral Aβ deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMHs) in the living human brain.

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We assessed whether the presence of juxtapapillary duodenal diverticula (JPDD) risks biliary stone disease and recurrence. In total, 695 patients who underwent ERCP were divided into two groups: biliary stone disease (group I, n = 523) and non-stone biliary diseases (group II, n = 172). Additionally, for a control group (group III), 80 age-matched healthy subjects underwent side-view duodenoscopy. In group I, rates of post-ERCP pancreatitis, cannulation failure, and disease recurrence in two-year follow up were compared according to the presence of JPDD. In results, the incidence of JPDD in group I (42.4%) was significantly higher than in group II (16.3%) and III (18.8%). The frequencies of JPDD were increased with age in all groups, and reached statistical significance in group I. In group I, rates of post-ERCP pancreatitis were significantly higher in patients with JPDD (18.5%) compared to JPDD negative (12.6%). The cannulation failure rate was also higher in patients with JPDD (9.9%) compared to JPDD negative (5.3%). Recurrence rate was higher in patients with JPDD (25.3%) compared to JPDD negative (9.2%). In conclusion, JPDD develops with aging and risks biliary stone formation. JPDD also seems to be associated with post-ERCP pancreatitis, cannulation failure and biliary stone recurrence.