Statins and Parkinson Disease Prognosis
Statins are more widely used not only for the primary and secondary prevention of cardiovascular disease by blocking cholesterol biosynthesis but also for the potential neuroprotective agents during neurological disorders due to their pleiotropic effects.
In this new study, the investigators studied whether the prior use of statins affect baseline nigrostriatal dopamine loss at the time of diagnosis and longitudinal motor and cognitive outcomes in patients with Parkinson's disease.
Five hundred drug-naïve patients with Parkinson's disease who underwent dopamine transporter imaging were classified into two groups according to the prior use of statins: patients with and without statin use. Multivariate linear regression was used to determine inter-group differences in dopamine transporter availability. We evaluated the longitudinal changes in levodopa-equivalent dose and dementia conversion between the groups using a linear mixed model and survival analysis, respectively. In addition, mediation analysis was applied to examine the effect of total cholesterol.
Patients with Parkinson's disease treated with statin had a lower baseline dopamine transporter availability in the anterior (2.13 ± 0.55 vs. 2.37 ± 0.67; p = 0.002), posterior (1.31 ± 0.43 vs. 1.49 ± 0.54; p = 0.003), and ventral putamina (1.40 ± 0.39 vs. 1.56 ± 0.47; p = 0.002) than that in matched patients with Parkinson's disease without statin.
Lnear regression models showed that a prior treatment of statin remained significantly and independently associated with more severely decreased dopamine transporter availability in the anterior putamen (Beta = -0.140, p = 0.004), posterior putamen (Beta = -0.162, p = 0.001), and ventral putamen (Beta = -0.140, p = 0.004).
A survival analysis showed that the rate of dementia conversion was significantly higher in patients with Parkinson's disease with statin (hazard ratio, 2.019; 95% CI, 1.108 - 3.678; P = 0.022) than those without statin.
This study suggests that statin use may have a detrimental effect on baseline nigrostriatal dopamine degeneration and long-term outcomes in patients with Parkinson's disease.