Abstract
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.
Highlights
Hyperuricemia is defined by the presence of serum uric acid levels above 6.8–7 mg/dL, and is associated with precipitation of monosodium urate (MSU) crystals in joints and development of gout, the most frequent inflammatory arthritis in developed countries [1]
6 mg/dL for defining hyperuricemia has been proposed, considering that the risk of gout increases when serum uric acid levels are above this threshold [1]. sUA levels are the result of the balance between dietary purine intake, xantine oxidase activity, and renal UA excretion [2]
The interaction between hyperuricemia and cognitive system is still debated, and results from studies are partly conflicting. It is debated whether there is a different interaction between sUA and cognitive function according to the type of dementia (Alzheimer’s—AD; Parkinson’s—PD; or vascular—VD)
Summary
Hyperuricemia is defined by the presence of serum uric acid (sUA) levels above 6.8–7 mg/dL, and is associated with precipitation of monosodium urate (MSU) crystals in joints and development of gout, the most frequent inflammatory arthritis in developed countries [1]. Even when serum uric acid is at high-normal level, this parameter may represent a predictor of cardiovascular adverse events. For these reasons, treating high sUA levels is pivotal for the optimal cardiovascular risk management [4]. The interaction between hyperuricemia and cognitive system is still debated, and results from studies are partly conflicting. It is debated whether there is a different interaction between sUA and cognitive function according to the type of dementia (Alzheimer’s—AD; Parkinson’s—PD; or vascular—VD). We discuss potential mechanisms that could explain this interaction, the possible role of diet, and future study directions aimed at improving the current knowledge
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