Statin therapy associated with a lower risk of Parkinson’s Disease
Exploring the Association between Statin Use and the Risk of Parkinson’s Disease: A Meta-Analysis of Observational Studies
Literature - Poly TN, Islam M, Walther BA, et al. - Neuroepidemiology 2017;49:142–151
Data on a possible association between statin therapy and Parkinson’s Disease (PD) are conflicting and inconclusive. Some studies showed that statins improve the symptoms and delay progression of PD, whereas other trials showed an increased risk of PD with statin use [1-4].
In this systematic review and meta-analysis of 13 observational studies, the possible association between statin use and PD risk was investigated. All studies were conducted between 2007 and 2016, and included 6 case-control studies and 7 cohort studies. All studies together included 4,877,059 subjects, out of which, 24,596 had PD. The methodological quality of the studies was assessed based on a modified version of the Newcastle-Ottawa Scale.
- Use of statins was significantly associated with a reduced risk of PD when compared with non-use. The overall pooled RR of PD in patients on statins was 0.70 (95%CI: 0.58–0.84). Significant heterogeneity was observed (I2 = 93.41%; P = 0.000; τ2 = 0.088).
- In 9 high quality eligible studies, an inversed risk of PD among statin users was found compared with non-users, with an RR of 0.66 (95%CI: 0.55–0.79), and significant heterogeneity (I2 = 72.91%; P = 0.000; τ2 = 0.043).
- 4 Poor quality studies showed an overall pooled RR of 0.86 (95%CI: 0.58–1.29) with significant heterogeneity (I2 = 97.99%; P = 0.000; τ2 = 0.145).
- In 4 studies assessing long-term risk (exposure of >3 years), the RR was 0.77 (95%CI: 0.55–1.07) with significant heterogeneity (I2 = 63.52%; P = 0.042; τ2 = 0.122).
- When compared with non-users, simvastatin, atorvastatin, and lovastatin were associated with a decreased risk of PD with RRs of 0.63 (95%CI: 0.47–0.84), 0.78 (95%CI: 0.71–0.85), and 0.89 (95%CI: 0.65–1.21), respectively, whereas pravastatin was associated with higher risk of PD (RR: 1.40; 95%CI: 0.79–2.50).
- The pooled RR for PD risk of case-control studies was 0.82 (95%CI: 0.63–1.07) in the random effects model with significant heterogeneity (I2 = 77.98%; P = 0.000; τ2 = 0.071), while for cohort studies it was 0.62 (95%CI: 0.50–0.79) with preserved heterogeneity (I2 = 94.71%; P = 0.000; τ2 = 0.073).
- Regional differences were seen, such that in 6 North American studies, the PD risk was lower in statin users than in 4 European studies, but 3 Asian studies showed the highest reduction of developing PD among statin users.
- A significant publication bias was observed (Egger’s regression test of funnel asymmetry, P <0.05).
In a meta-analysis of 13 observational studies, statin use was associated with a modest reduction in the risk of developing Parkinson’s Disease compared with not using statins. When interpreting this result, the significant statistical and clinical heterogeneity among the included studies should be taken into account, as well as publication bias. No exact potential pathological hypothesis has been postulated that could explain how statin use may reduce the onset of PD. More experimental models are needed to help identifying a possible biological mechanism of these observations.