Association of serum uric acid levels with bone mineral density and the presence of osteoporosis in Chinese patients with Parkinson's disease: a cross-sectional study.

INTRODUCTION: As the population ages, the incidence of osteoporosis among patients suffering from Parkinson's disease (PD) will surge continually, and the ensuing disability from falls is becoming a serious social burden. Due to its antioxidant properties, much literature has indicated the possible ability of serum uric acid (UA) to prevent ageing-related diseases caused by oxidative stress, including osteoporosis and PD. Therefore, this study was for exploring the connection of serum UA levels with bone mineral density (BMD) and the osteoporosis presence in Chinese PD patients. MATERIALS AND METHODS: A cross-sectional design was used to statistically analyze 42 clinical parameters obtained from 135 patients with PD treated in Wuhan Tongji Hospital during 2020-2022. Multiple stepwise linear regression and multiple logistic regression analyses were constructed for identifying the association of serum UA levels with BMD as well as osteoporosis in PD patients, respectively. With receiver operative characteristic (ROC) curves, the optimal cutoff value was acquired for serum UA in the diagnosis of osteoporosis. RESULTS: According to the regression analysis adjusted for confounders, serum UA levels in PD patients had positive correlation with BMD at each site and negative correlation with the presence of osteoporosis (P < 0.05 for all). ROC curves determined that the optimal cutoff value for UA to perform well in diagnosing osteoporosis in PD patients was 284.27 µmol/L (P < 0.001). CONCLUSION: Relatively higher serum UA levels in the physiological range can work as a biomarker of higher BMD, and were strongly linked to lower prevalence of osteoporosis in Chinese PD patients.

Cross-sectional study and bioinformatics analysis to reveal the correlations of osteoporosis in patients with Parkinson's disease.

OBJECTIVES: Osteoporosis and Parkinson's disease (PD) are both aging-related diseases. PD patients with comorbid osteoporosis are vulnerable to the risk of fracture, which leads to a serious public health burden to the whole society. Therefore, this study sought to reveal the clinical and genetic correlations between PD and osteoporosis based on a cross-sectional study and bioinformatics analysis. METHODS: A cross-sectional study of 95 PD patients and 99 healthy controls was conducted. Ordinal logistic regression analysis was utilized to investigate the clinical correlations between PD and osteoporosis. Two microarray datasets (GSE20292, GSE35958) including PD, osteoporosis and normal control samples were retrieved from the GEO database for GO analysis, KEGG pathway analysis and PPI network. RESULTS: PD patients had lower 25(OH)VitD, FN BMD, BMD and T-score of the LS and TH, as well as poorer bone mass diagnosis, yet higher PINP compared to healthy controls. Both age and UPDRS II score of PD patients were adversely correlated with BMD of LS and TH. PD diagnosis acted as an independent risk factor of osteoporosis, and PD patients had approximately double risk for osteoporosis. Bioinformatics analysis further revealed that SNAP25, AQP4, SV2B, KCND3, and ABCA2 had important diagnostic value and risk prediction value for both PD and osteoporosis. CONCLUSIONS: PD diagnosis can be used as an independent risk factor for osteoporosis. Moreover, SNAP25, AQP4, SV2B, KCND3 and ABCA2 as the top 5 hub genes have important diagnostic and risk predictive value for both PD and osteoporosis.

Sphingosine-1-phosphate related signalling pathways manipulating virus replication.

Viruses can create a unique cellular environment that facilitates replication and transmission. Sphingosine kinases (SphKs) produce sphingosine-1-phosphate (S1P), a bioactive sphingolipid molecule that performs both physiological and pathological effects primarily by activating a subgroup of the endothelial differentiation gene family of G-protein coupled cell surface receptors known as S1P receptors (S1PR1-5). A growing body of evidence indicates that the SphK/S1P axis is crucial for regulating cellular activities in virus infections like respiratory viruses, enteroviruses, hepatitis viruses, herpes viruses, and arboviruses replicate. Depending on the type of virus, pro- or anti-viral activities of the SphK/S1P axis sometimes rely on the host immune system and sometimes directly through intracellular signalling pathways or cell proliferation. Recent research has shown novel roles of S1P and SphK in viral replication. Sphingosine kinase isoforms (SphK1 and SphK2) levels can be manipulated by several viruses to promote the effects that are expected. Regulation of cellular signalling pathways plays a significant role in the mechanism. The purpose of this review is to provide insight of the characters played by the SphK/S1P axis throughout diverse viral infection processes. We then assess potential therapeutic methods that are based on S1P signalling and metabolism during viral infections.