Uric Acid and Cognitive Function in Older Individuals

Tana, Claudio; Ticinesi, Andrea; Prati, Beatrice; Nouvenne, Antonio; Meschi, Tiziana

doi:10.3390/nu10080975

Cited by 115 publications

(93 citation statements)

References 73 publications

(82 reference statements)

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“…Despite high heterogeneity in the existing studies, serum uric acid may modulate cognitive function differently according to the etiology of dementia [52]. In this study, hyperhomocysteinemia and hyperuricemia were observed in dementia subtypes with vascular lesions (AD with CVD and vascular dementia).…”

Section: Discussionmentioning

confidence: 72%

“…Current research proves that uric acid can act as a nerve protection against Alzheimer's disease and Parkinson's disease dementia, and hyperuricemia represents a risk factor that indicates the rapid progress of the disease and possible signs of malnutrition [8]. It is known that high uric acid can exert beneficial functions due to its antioxidant properties, which may be particularly relevant in the context of neurodegenerative diseases [52]. However, recent studies have suggested that these two markers are associated with an increased risk of vascular disease [13,53].…”

Section: Discussionmentioning

confidence: 99%

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The Different Relationship between Homocysteine and Uric Acid Levels with Respect to the MTHFR C677T Polymorphism According to Gender in Patients with Cognitive Impairment

et al. 2020

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In an elderly population with cognitive impairment, we investigated the association between serum uric acid (sUA) and serum homocysteine (sHcy), known risk factors for cerebrovascular disease. We also investigated the potential effect of the C677T polymorphism in the gene encoding methylenetetrahydrofolate reductase (MTHFR) to the sUA level in different dementia types. Participants underwent a battery of tests including measurements of sUA, sHcy, folic acid, and vitamin B12 as well as genotyping of the MTHFR locus. Data from 861 subjects (597 females to 264 males) were retrospectively analyzed. Subjects with hyperhomocysteinemia had lower serum folic acid and vitamin B12 and higher sUA than those with normal sHcy. sUA was significantly associated with serum creatinine, HbA1c, and sHcy regardless of gender. The TT genotype was found to be associated with hyperhomocysteinemia in both genders (p = 0.001). The levels of hyperlipidemia, sHcy, and sUA differed according to dementia subtypes. High sUA were associated with hyperhomocystenemia in TT genotype only in dementia with vascular lesion. This study reveals that sUA is positively associated with sHcy. We speculate that the two markers synergistically increase cerebrovascular burden and suggested that dietary intervention for sUA and sHcy would be helpful for cognitive decline with vascular lesion.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

The Different Relationship between Homocysteine and Uric Acid Levels with Respect to the MTHFR C677T Polymorphism According to Gender in Patients with Cognitive Impairment

et al. 2020

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“…Urate, a metabolite of purine nucleotides, is an antioxidant in blood and brain tissue that exerts neuroprotective effects by scavenging reactive oxygen species [ 9 , 10 ]. Although urate has been associated with cognitive function in older people, the data is somewhat conflicting and may depend on the aetiology of the dementia, with protective effects being observed in Parkinson’s dementia and Alzheimer’s disease, but not in vascular dementia [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Positive Association of Ascorbate and Inverse Association of Urate with Cognitive Function in People with Parkinson’s Disease

et al. 2020

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Oxidative stress is thought to contribute to the aetiology of neurological disorders such as Parkinson’s disease. Ascorbate (vitamin C) is a potent antioxidant and is associated with neurological and cognitive function. In this study we assessed the ascorbate status of a cohort of people with Parkinson’s disease (n = 215), aged 50–90 years, compared with a cohort of age matched healthy controls (n = 48). The study sample’s cognitive status ranged from normal to mild cognitive impairment and dementia. There was no difference between the Parkinson’s disease and healthy control groups with respect to mean ascorbate status, however, a higher proportion of participants with Parkinson’s disease had hypovitaminosis C (i.e., <23 μmol/L) compared with healthy controls (20% vs. 8%, respectively). Within the Parkinson’s disease group, Montreal Cognitive Assessment (MoCA) scores correlated positively with ascorbate concentrations, with higher ascorbate status associated with better cognitive function (r = 0.14, p = 0.045). Participants with hypovitaminosis C had significantly lower MoCA scores relative to participants with ascorbate concentrations >23 µmol/L (p = 0.014). Ascorbate concentrations were significantly lower in the cognitively impaired subgroup compared with the normal cognition subgroup in the Parkinson’s disease cohort (p = 0.03). In contrast, urate showed an inverse correlation with cognitive function (r = −0.19, p = 0.007), with higher urate concentrations observed in the cognitively impaired subgroup compared with the normal cognition subgroup (p = 0.015). There was an inverse association between ascorbate status and urate concentrations (r = −0.15, p = 0.017). Plasma protein carbonyls, a measure of systemic oxidative stress, were not significantly different between the Parkinson’s disease cohort and healthy controls, and there was no association with cognitive function (r = 0.09, p = 0.19) or with ascorbate status (r = −0.05, p = 0.45). Overall, our study showed ascorbate status was positively associated with cognitive function in Parkinson’s disease, suggesting that longitudinal studies investigating the temporal sequence of cognitive decline and ascorbate status are warranted.

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“…Recent reviews and meta-analysis studies focused on the role of uric acid in dementia/cognitive impairment related to senescence, suggesting that uric acid has a protective action in Alzheimer's disease and Parkinson's dementia (hydrophilic antioxidant properties), while hyperuricemia may have a negative influence during vascular dementia (stroke, small vessel cerebrovascular disease) [86,87].…”

Section: Clinical Reportsmentioning

confidence: 99%

Pro-Aging Effects of Xanthine Oxidoreductase Products

et al. 2020

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The senescence process is the result of a series of factors that start from the genetic constitution interacting with epigenetic modifications induced by endogenous and environmental causes and that lead to a progressive deterioration at the cellular and functional levels. One of the main causes of aging is oxidative stress deriving from the imbalance between the production of reactive oxygen (ROS) and nitrogen (RNS) species and their scavenging through antioxidants. Xanthine oxidoreductase (XOR) activities produce uric acid, as well as reactive oxygen and nitrogen species, which all may be relevant to such equilibrium. This review analyzes XOR activity through in vitro experiments, animal studies and clinical reports, which highlight the pro-aging effects of XOR products. However, XOR activity contributes to a regular level of ROS and RNS, which appears essential for the proper functioning of many physiological pathways. This discourages the use of therapies with XOR inhibitors, unless symptomatic hyperuricemia is present.

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Uric Acid and Cognitive Function in Older Individuals

Cited by 115 publications

References 73 publications

The Different Relationship between Homocysteine and Uric Acid Levels with Respect to the MTHFR C677T Polymorphism According to Gender in Patients with Cognitive Impairment

The Different Relationship between Homocysteine and Uric Acid Levels with Respect to the MTHFR C677T Polymorphism According to Gender in Patients with Cognitive Impairment

Positive Association of Ascorbate and Inverse Association of Urate with Cognitive Function in People with Parkinson’s Disease

Pro-Aging Effects of Xanthine Oxidoreductase Products

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