Dear Editor,

Li et al. conducted a meta-analysis to evaluate the association between serum uric acid (UA), vascular dementia (VaD), and Parkinson’s disease dementia (PDD) [1]. There was an inverse relationship between serum UA levels and PDD but not a significant relationship with VaD. I present some information regarding the association between serum UA and dementia subtypes.

First, González-Aramburu et al. reported that there was no significant association between serum UA levels and the risk of PDD with special reference to genetic variants [2], which was not inconsistent with data by Li et al. I suppose that genotypes of PD and the level of progression may be varied in this type of dementia, and an enough number of samples are needed to conduct a stratified analysis to specify the relationship between serum UA and PDD.

Second, Latourte et al. conducted a prospective study to investigate the serum UA level on the incidence of dementia by the median follow-up of 10 years [3]. The adjusted hazard ratio (95% CI) of the highest versus lowest serum UA level for vascular or mixed dementia and Alzheimer’s disease was 3.66 (1.29 to 10.41) and 1.55 (0.92 to 2.61), respectively. In contrast, Scheepers et al. conducted a long follow-up study with mean periods of 33 years, and the adjusted HR (95% CI) of higher serum UA for Alzheimer’s disease and VaD were 0.78 (0.66–0.91) and 0.66 (0.47–0.94), respectively [4]. This means that follow-up periods may contribute to the association of serum UA with the risk of dementia, which should be paid attention for a meta-analysis.

Finally, high serum UA is significantly associated with increased number of metabolic components and the risk of cardiovascular diseases, which would increase the risk of atherosclerotic disorders [5]. In contrast, ischemic changes in the brain may lead to reduce the levels of UA. As serum UA has a neuron-protective effect in patients with acute ischemic stroke, there is an advantage of increased serum UA in patients with ischemic stroke. To reduce the infarct growth and improve in the behavioral dysfunction, the patients’ body needs serum UA for a therapeutic action [6]. Namely, there is a possibility that reduced serum UA might be caused by the need to repair brain damage and reduce the development of VaD. This speculation should be checked by further experimental studies [7].