Objective Using a large US claims database (MarketScan®), we investigated the controversy surrounding the role of statins in Parkinson’s disease (PD). Methods We performed a retrospective case-control analysis. First, we identified 2,322 incident PD cases having a minimum of 2.5 y of continuous enrollment prior to earliest diagnosis code or prescription of antiparkinson medication. Then, 2,322 Controls were matched individually by age, gender, and a “follow-up window” to explore the relationship of statin use with incident PD. Results Statin usage was significantly associated with PD risk, with the strongest associations being for lipophilic (OR=1.58, p<0.0001) vs. hydrophilic (OR=1.19, p=0.25) statins, statins plus non-statins (OR=1.95, p<0.0001), and for the initial period after starting statins (<1 y OR=.82, 1–2.5 y OR =1.75, and ≥2.5 y OR =1.37; ptrend<0.0001). Conclusion Use of statin (especially lipophilics) was associated with higher risk of PD, and the stronger association in initial use suggests a facilitating effect.

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Background Cortical and subcortical gray matter (GM) atrophy may progress differently during the course of Parkinson's disease (PD). We delineated and compared the longitudinal pattern of these PD-related changes. Methods Structural MRIs and clinical measures were obtained from 76 PD with different disease durations and 70 Controls at baseline, 18- and 36-months. Both cortical and subcortical (putamen, caudate, and globus pallidus) GM volumes were obtained, compared, and associated with PD clinical measures at baseline. Their volumes and rates of change also were compared among Controls, PDs, and PD subgroups based on duration of illness [≤1 year (PDE), 1-5 years (PDM), and >5 years (PDL)]. Results Compared to Controls, PD subjects displayed smaller cortical GM and striatal (putamen, caudate, ps≤0.001), volumes at baseline. Cortical GM volumes were negatively associated with disease duration at baseline, whereas striatal volumes were not. PD subjects demonstrated accelerated volume loss in cortical GM (p=0.006), putamen (p=0.034), and caudate (p=0.008) compared to Controls. Subgroup analyses demonstrated that accelerated cortical atrophy reached statistical significance in PD subjects with duration of illness 1-5 years (PDM, ps<0.001) and the trend of accelerated atrophy seemed to persist until later stages, whereas striatal atrophy occurred in PD subjects with PDE (p=0.021 for putamen, p=0.005 for caudate) and PDM (p=0.002 for putamen, p=0.001 for caudate) that significantly slowed down in PDL (ps for PDL vs PDE or PDM: <0.01). Conclusions The pattern of GM loss in PD differs in cortical and subcortical regions, with striatal atrophy occurring earlier and extra-striatal cortical atrophy later.