In the vast realm of scientific research, one question has captivated scientists for years: do psychiatric disorders have a causal relationship with Parkinson’s Disease (PD), or is it all a coincidence? A team of researchers took on this challenge by conducting a bidirectional Mendelian randomization (MR) study. They delved into the massive amount of public data from genome-wide association studies (GWAS) on both psychiatric disorders and PD. Using advanced statistical methods like MR-PRESSO and IVW, they explored potential causal links between these conditions. While the forward MR analysis didn’t provide definitive evidence, the reverse analysis revealed an intriguing finding – a causal relationship between PD and bipolar disorder. Further analyses even showed that genetically predicted PD could increase the risk of developing certain bipolar disorder subtypes. The absence of pleiotropy and heterogeneity in the study further supports these results. This study contributes to our understanding of the complex interplay between psychiatric disorders and PD, shedding light on how these conditions may influence each other. To learn more about this groundbreaking research, dive into the full article!

IntroductionAlthough the relationship between psychiatric disorders and Parkinson’s disease (PD) has attracted continuous research attention, the causal linkage between them has not reached a definite conclusion.MethodsTo identify the causal relationship between psychiatric disorders and PD, we used public summary-level data from the most recent and largest genome-wide association studies (GWASs) on psychiatric disorders and PD to conduct a bidirectional two-sample Mendelian randomization (MR). We applied stringent control steps in instrumental variable selection using the Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) method to rule out pleiotropy. The inverse-variance weighted (IVW) method was used to identify the causal relationship between psychiatric disorders and PD. Multiple MR analysis methods, including MR-Egger, weighted-median, and leave-one-out analyses, were used for sensitivity analysis, followed by heterogeneity tests. Further validation and reverse MR analyses were conducted to strengthen the results of the forward MR analysis.ResultsThe lack of sufficient estimation results could suggest a causal relationship between psychiatric disorders and PD in the forward MR analysis. However, the subsequent reverse MR analysis detected a causal relationship between PD and bipolar disorder (IVW: odds ratios [OR] =1.053, 95% confidence interval [CI] =1.02–1.09, p = 0.001). Further analysis demonstrated a causal relationship between genetically predicted PD and the risk of bipolar disorder subtype. No pleiotropy or heterogeneity was detected in the analyses.DiscussionOur study suggested that while psychiatric disorders and traits might play various roles in the risk of developing PD, PD might also be involved in the risk of developing psychiatric disorders.

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