ArticleIBRO neuroscience reports2024
Correlation between 25-hydroxy-vitamin D and Parkinson's disease.
Article in IBRO neuroscience reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effect of vitamin D supplementation on motor symptoms in Parkinson's disease: a meta-analysis of randomized controlled trials.Frontiers in nutrition · 2025Pooled it
- Article
- Vitamin D Signaling in Neurodegenerative Disorders: Mechanisms, Therapeutic Potential, and Clinical Implications.Nutrients · 2026Review
- Cadmium-Induced Toxicity as a Pathophysiological Mechanism for Parkinson's Disease Onset in Individuals with Iron and Zinc Deficiencies and Chronic Obstructive Pulmonary Disease.Neurology international · 2026Review
- Vitamin D and Brain Health.Advances in experimental medicine and biology · 2026Review
- The Role of Vitamin D in Parkinson's Disease: Evidence from Serum Concentrations, Supplementation, andNeuroSci · 2025Review
- The quest for Parkinson's disease biomarkers: traditional and emerging multi-omics approaches.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Previous cross-sectional studies have shown that Parkinson's disease (PD) patients have lower serum 25-hydroxyvitamin D (25(OH)D) concentrations than controls. Other studies have not yet tested whether research findings from other regions are generalizable to Chinese populations. In this case-control study, we examined the correlation between 25-hydroxyvitamin D and Parkinson's disease. Methods: We established an association between 25-hydroxyvitamin D deficiency and PD in a case-control study of 100 PD patients and 100 control subjects free of neurological disease at the First Affiliated Hospital of Xinjiang Medical University. Results: Total 25-hydroxyvitamin D levels were deficient in 21 % of patients with PD compared with 4 % of controls. In univariate analyses, plasma levels of 25-hydroxyvitamin D were associated with PD (p < 0.001). In multivariate analyses, vitamin D deficiency (25(OH)D < 20 ng/mL) was significantly associated with PD (p = 0.008, Odds Ratio =17.13, 95 % CI= 2.082-141.075). Individuals with 25(OH)D levels in the lowest quartile had the highest prevalence of PD (p = 0.026, OR=11.786, 95 % CI =1.342-103.51 compared to individuals with values in the highest quartile). Conclusions: Our study reveals an association between 25-hydroxyvitamin D and PD. Patients with incident PD had significantly lower serum 25(OH)D concentrations than age-matched controls. High-risk PD patients with vitamin D deficiency who have not yet developed exercise impairment should undergo vitamin D measurement and any necessary treatment as soon as possible. Limitations of the study: the study needs further assessment of populations with low vitamin D levels in other regions of China; further assessment of the effect of different sources of vitamin D on PD; further study of longitudinal cohorts at different time points.
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