Abstract
Aim. To pool the data currently available to determine the association between calcium channel blockers (CCBs) and risk of Parkinson's disease (PD). Methods. Literature search in PubMed, EBSCO, and Cochrane library was undertaken through March 2014, looking for observational studies evaluating the association between CCBs use and PD. Pooled relative risk (RR) estimates and 95% confidence intervals (CIs) were calculated using random-effects model. Subgroup analyses, sensitivity Analysis, and cumulative meta-analysis were also performed. Results. Six studies were included in our meta-analysis according to the selection criteria, including three cohort studies and three case-control studies involving 27,67,990 subjects including 11,941 PD cases. We found CCBs use was associated with significant decreased risk of PD, compared with not using CCBs (random effects model pooled RR, 0.81 (95% CI, 0.69–0.95)); a significant heterogeneity was found between studies (P = 0.031; I 2 54.6%). Both the classes of CCB, that is, dihydropyridine calcium channel blockers (DiCCB) (0.80 (95% CI, 0.65–0.98) P = 0.032) and non-DiCCB (0.70 (95% CI, 0.53–0.92) P = 0.013), were found to be reducing the risk of PD. Conclusion. In our analysis, we found that CCBs use was associated with a Significantly decreased risk of PD compared with non-CCB use.
Highlights
1% of the population over 60 years of age suffers from Parkinson’s disease (PD) which is a second most common chronic progressive neurodegenerative disorder in the elderly after Alzheimer’s disease [1]
We found calcium channel blockers (CCBs) use was associated significantly with decreased risk of PD compared with not using CCB (pooled relative risk (RR), 0.81)
The present analysis demonstrated the potential neuroprotective role of CCBs in reducing the risk of PD
Summary
1% of the population over 60 years of age suffers from Parkinson’s disease (PD) which is a second most common chronic progressive neurodegenerative disorder in the elderly after Alzheimer’s disease [1]. It has been characterized clinically by three motor symptoms, which includes resting tremors, rigidity, and bradykinesia [2]. A systematic review suggests that the centrally acting calcium channel blockers (CCBs) may have disease-modifying effects, and there were no drugs to prevent the disease or slow its progression [4]. Experiments in animal models indicated that the voltagegated calcium channel subtype Ca (V) 1.3 has a function in making neurons vulnerable to neurodegeneration [6]
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