scholarly journals Association between Serum Uric Acid Levels and Alzheimer’s Disease: A Meta Analysis

2018 ◽  
Vol 08 (03) ◽  
pp. 356-365
Author(s):  
雨涵 王
PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94084 ◽  
Author(s):  
Xueping Chen ◽  
Xiaoyan Guo ◽  
Rui Huang ◽  
Yongping Chen ◽  
Zhenzhen Zheng ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Mengyuan Qiao ◽  
Chongli Chen ◽  
Yuqing Liang ◽  
Yuxi Luo ◽  
Wenbin Wu

As a powerful antioxidant in the human body, uric acid (UA) has been the subject of increasing research that focused on its influence on Alzheimer’s disease (AD) in recent years. The latest literature was gathered to describe the influence of serum uric acid (SUA) level on the onset and progression of AD and to analyze the possibility that SUA is a biomarker of Alzheimer’s disease. A large number of existing studies suggested that the SUA level was lower or tended to decrease in patients with AD, and increased SUA level may have a protective effect in AD, which could reduce the risk of onset and slowing the course of the disease. However, some Mendelian randomization analyses suggested that genetically determined uric acid was not associated with AD risk. Existing research results are contradictory due to the high inconsistency of the studies, the selection of subjects, and other factors. UA also showed a strong association with cognitive function, and there appeared to be a gender-selective neuroprotective action. Due to its potent antioxidant properties, the low uric acid level may contribute to oxidative stress to accelerate disease progression. But some preclinical data showed a possibility that in some special cases, UA had a prooxidant properties. The possibility was raised in the discussion of the underlying mechanism that both the low uric acid level and the rapidly progressive course of the disease were the consequence of malnutrition. This paper reviews recent advances in the study of SUA and AD which offers the possibility of new biomarker, new prevention, and treatment strategies for Alzheimer’s disease.


2015 ◽  
Vol 11 (7S_Part_14) ◽  
pp. P657-P658
Author(s):  
Byoung Seok Ye ◽  
Young H. Sohn ◽  
Jee Hyun Ham ◽  
Jae Jung Lee ◽  
Won Woo Lee ◽  
...  

2017 ◽  
Vol 33 (2) ◽  
pp. 83-88
Author(s):  
Mohammad Saifullah Ahtesam ◽  
Md Ahsan Habib ◽  
Md Rafiqul Islam ◽  
Md Rezaul Karim Khan ◽  
Hasan Zahidur Rahman ◽  
...  

Background: Alzheimer’s disease is the most common cause of dementia. Uric acid is the end product of purine metabolism in humans and acts as a natural antioxidant, accounting up to 60% of the free radical scavenging activity in human blood to prevent free radicals induced oxidative cell injury. This study aimed to explore the association between serum uric acid level and cognitive impairment of Alzheimer’s disease patients compared to those of the non-demented age and sex matched controls. Methods: This case control study was carried out in the department of neurology, BSMMU, Dhaka. Total 116 patients were enrolled as study population after satisfying inclusion and exclusion criteria. Among them, 58 were grouped as case and rest 58 were control. All blood samples for serum uric acid were measured in the Biochemistry lab, Department of Biochemistry, BSMMU, Dhaka. Results: A signiûcant reduction of serum uric acid levels in the AD group was found compared to those of the control group (4.35±1.59 Vs 6.89±1.68) which was statistically significant (p<0.001). We also found a positive correlation between serum uric acid levels with severity of Alzheimer’s disease (rp = 0.633, P<0.001). Among demographic variables educational qualification was statistically significant (p=0.006) in AD patients. Conclusion: This study showed that oxidative injuries have an important role in the pathogenesis of AD. Higher levels of uric acid are associated with a decreased risk of dementia and better cognitive function later in life. Bangladesh Journal of Neuroscience 2017; Vol. 33 (2): 83-88


2021 ◽  
pp. 1-13
Author(s):  
Lin-Lin Li ◽  
Ya-Hui Ma ◽  
Yan-Lin Bi ◽  
Fu-Rong Sun ◽  
Hao Hu ◽  
...  

Background: Serum uric acid (SUA) affects the reaction of oxidative stress and free radicals in the neurodegenerative processes. However, whether SUA impacts Alzheimer’s disease (AD) pathology remains unclear. Objective: We aimed to explore whether high SUA levels can aggravate the neurobiological changes of AD in preclinical AD. Methods: We analyzed cognitively intact participants (n = 839, age 62.16 years) who received SUA and cerebrospinal fluid (CSF) biomarkers (amyloid-β [Aβ], total tau [t-Tau], and phosphorylated tau [p-Tau]) measurements from the Chinese Alzheimer’s Biomarker and LifestylE (CABLE) database using multivariable-adjusted linear models. Results: Levels of SUA in the preclinical AD elevated compared with the healthy controls (p = 0.007) and subjects with amyloid pathology had higher concentration of SUA than controls (p = 0.017). Roughly, equivalent levels of SUA displayed among cognitively intact individuals with or without tau pathology and neurodegeneration. CSF Aβ1 - 42 (p = 0.019) and Aβ1 - 42/Aβ1 - 40 (p = 0.027) were decreased and CSF p-Tau/Aβ1 - 42 (p = 0.009) and t-Tau/Aβ1 - 42 (p = 0.043) were increased with the highest (>  75th percentile) SUA when compared to lowest SUA, implying a high burden of cerebral amyloidosis in individuals with high SUA. Sensitivity analyses using the usual threshold to define hyperuricemia and precluding drug effects yielded robust associations. Nevertheless, the quadratic model did not show any U-shaped relationships between them. Conclusion: SUA may aggravate brain amyloid deposition in preclinical AD, which corroborated the detrimental role of SUA.


2016 ◽  
Vol 12 ◽  
pp. P1059-P1059
Author(s):  
Byoung Seok Ye ◽  
Woo Seok Ha ◽  
Jae Jung Lee ◽  
Yoonju Lee ◽  
Phil Hyu Lee ◽  
...  

Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 975 ◽  
Author(s):  
Claudio Tana ◽  
Andrea Ticinesi ◽  
Beatrice Prati ◽  
Antonio Nouvenne ◽  
Tiziana Meschi

Hyperuricemia has been recognized as an independent cardiovascular risk factor in epidemiological studies. However, uric acid can also exert beneficial functions due to its antioxidant properties, which may be particularly relevant in the context of neurodegenerative diseases. In this paper, we critically revise the evidence on the relationship between serum uric acid levels and cognitive function in older individuals, focusing on the etiology of cognitive impairment (Alzheimer’s disease, Parkinson’s dementia, and vascular dementia) and on the interactive connections between uric acid, dementia, and diet. Despite high heterogeneity in the existing studies, due to different characteristics of studied populations and methods of cognitive dysfunction assessment, we conclude that serum uric acid may modulate cognitive function in a different way according to the etiology of dementia. Current studies indeed demonstrate that uric acid may exert neuroprotective actions in Alzheimer’s disease and Parkinson’s dementia, with hypouricemia representing a risk factor for a quicker disease progression and a possible marker of malnutrition. Conversely, high serum uric acid may negatively influence the disease course in vascular dementia. Further studies are needed to clarify the physio-pathological role of uric acid in different dementia types, and its clinical-prognostic significance.


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