Uric acid is commonly known for its bad reputation. However, it has been shown that uric acid may be actively involved in neurotoxicity and/or neuroprotection. These effects could be caused by oxidative stress or inflammatory processes localized in the central nervous system, but also by other somatic diseases or systemic conditions. Our interest was to summarize and link the current data on the possible role of uric acid in cognitive functioning. We also focused on the two putative molecular mechanisms related to the pathological effects of uric acid—oxidative stress and inflammatory processes. The hippocampus is a prominent anatomic localization included in expressing uric acid's potential impact on cognitive functioning. In neurodegenerative and mental disorders, uric acid could be involved in a variety of ways in etiopathogenesis and clinical presentation. Hyperuricemia is non-specifically observed more frequently in the general population and after various somatic illnesses. There is increasing evidence to support the hypothesis that hyperuricemia may be beneficial for cognitive functioning because of its antioxidant effects but may also be a potential risk factor for cognitive dysfunction, in part because of increased inflammatory activity. In this context, gender specificities must also be considered.
Oxidative stress and neuroinflammation have a role in the pathogenesis of multiple sclerosis (MS) and in depression. Fatigue is the most disabling symptom in patients with MS and could also be a part of depressive symptomatology. In this study, we measured the serum levels of uric acid (UA) as a marker of oxidative stress and C-reactive protein (CRP) as an inflammatory marker, in 98 patients with MS in relapse and remitting phase of illness and 35 healthy subjects. Degree of depressive symptomatology and fatigue were assessed with Beck's Depression Inventory (BDI) and Fatigue Severity Scale (FSS). Further, we examined the possible correlation of these biomarkers with symptoms of depression and fatigue. Relapse and remitting MS had a lower serum UA levels than controls (236.97 ± 9.25 µmol/L vs. 268.27 ± 0.09 µmol/L vs. 314.82 ± 11.02 µmol/L; p = 0.000), while sera levels of CRP were higher in relapse than remitting patients (4.46 ± 0.40 mg/L vs. 1.01 ± 0.38 mg/L; p = 0.000). Patients in relapse had higher BDI scores (15.68 ± 16.62 vs. 8.36 ± 7.10; p = 0.045). Decreased UA levels showed weak negative correlation with the presence of sadness and disturbed daily activities, higher CRP levels positively correlated with severe depression and the correlation between depression and fatigue was also observed (p < 0.05). It is possible that decreased UA levels lead to sadness, disturbed daily activities and severe disability. Every attack of CRP elevation in relapse could additionally precipitate the depression onset. The clinicians must pay special attention to early detection of fatigue because it could precede depression and improve further treatment.
Uric acid (UA) has been shown to have neuroprotective or neurotoxic properties, in relation to specific tissues and diseases that have been studied. Previous studies provided contradictory results on the role of UA in schizophrenia as a neurodegenerative disorder. The aim of this brief report was an additional analysis of UA sera levels in different phases of schizophrenia. Here, 86 patients with first-episode psychosis (FEP) vs. 45 patients with schizophrenia in relapse (SC in relapse) vs. 35 healthy control subjects (HC) were studied before and 1 month after antipsychotic therapy. Further, we aimed to explore the possible correlation of UA with scores presenting clinical features and with serum concentrations of the proinflammatory cytokines interleukin (IL)-6 and IL-17. When comparing the data between all three groups, we did not find significant differences in UA levels, either before or after the applied therapy. Also, comparing sera concentrations of UA in every single group, the analysis did not reveal statistically significant differences between FEP patients, but statistically, a significant difference was found in SC in relapse before and after treatment (334.71 ± 116.84 vs. 289.37 ± 109.15 μmol/L, p = 0.05). Uric acid serum levels correlated with negative sub-score (p = 0.001, r = 0.306), general sub-score (p = 0.015, r = 0.236), and total PANSS score (p = 0.009, r = 0.3) after 1 month of therapy. We have established a statistically significant positive correlation between serum concentrations of UA and IL-6 in exacerbation (p = 0.01, r = 0.220) and with IL-17 after treatment and in the stabilization of psychosis (p = 0.01, r = 0.34), suggesting potential cascades in different phases of schizophrenia that potentiate inflammation.
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