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001     270631
005     20240718121108.0
024 7 _ |a 10.1212/WNL.0000000000209620
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024 7 _ |a 0028-3878
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024 7 _ |a 1526-632X
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037 _ _ |a DZNE-2024-00803
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Domenighetti, Cloé
|0 0000-0001-6408-0351
|b 0
245 _ _ |a Association of Body Mass Index and Parkinson Disease: A Bidirectional Mendelian Randomization Study.
260 _ _ |a [Erscheinungsort nicht ermittelbar]
|c 2024
|b Ovid
336 7 _ |a article
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336 7 _ |a Journal Article
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a The role of body mass index (BMI) in Parkinson disease (PD) is unclear. Based on the Comprehensive Unbiased Risk Factor Assessment for Genetics and Environment in PD (Courage-PD) consortium, we used 2-sample Mendelian randomization (MR) to replicate a previously reported inverse association of genetically predicted BMI with PD and investigated whether findings were robust in analyses addressing the potential for survival and incidence-prevalence biases. We also examined whether the BMI-PD relation is bidirectional by performing a reverse MR.We used summary statistics from a genome-wide association study (GWAS) to extract the association of 501 single-nucleotide polymorphisms (SNPs) with BMI and from the Courage-PD and international Parkinson Disease Genomics Consortium (iPDGC) to estimate their association with PD. Analyses are based on participants of European ancestry. We used the inverse-weighted method to compute odds ratios (ORIVW per 4.8 kg/m2 [95% CI]) of PD and additional pleiotropy robust methods. We performed analyses stratified by age, disease duration, and sex. For reverse MR, we used SNPs associated with PD from 2 iPDGC GWAS to assess the effect of genetic liability toward PD on BMI.Summary statistics for BMI are based on 806,834 participants (54% women). Summary statistics for PD are based on 8,919 (40% women) cases and 7,600 (55% women) controls from Courage-PD, and 19,438 (38% women) cases and 24,388 (51% women) controls from iPDGC. In Courage-PD, we found an inverse association between genetically predicted BMI and PD (ORIVW 0.82 [0.70-0.97], p = 0.012) without evidence for pleiotropy. This association tended to be stronger in younger participants (≤67 years, ORIVW 0.71 [0.55-0.92]) and cases with shorter disease duration (≤7 years, ORIVW 0.75 [0.62-0.91]). In pooled Courage-PD + iPDGC analyses, the association was stronger in women (ORIVW 0.85 [0.74-0.99], p = 0.032) than men (ORIVW 0.92 [0.80-1.04], p = 0.18), but the interaction was not statistically significant (p-interaction = 0.48). In reverse MR, there was evidence for pleiotropy, but pleiotropy robust methods showed a significant inverse association.Using an independent data set (Courage-PD), we replicate an inverse association of genetically predicted BMI with PD, not explained by survival or incidence-prevalence biases. Moreover, reverse MR analyses support an inverse association between genetic liability toward PD and BMI, in favor of a bidirectional relation.
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588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Mendelian Randomization Analysis
|2 MeSH
650 _ 2 |a Parkinson Disease: genetics
|2 MeSH
650 _ 2 |a Parkinson Disease: epidemiology
|2 MeSH
650 _ 2 |a Body Mass Index
|2 MeSH
650 _ 2 |a Polymorphism, Single Nucleotide: genetics
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Genome-Wide Association Study
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Risk Factors
|2 MeSH
700 1 _ |a Sugier, Pierre-Emmanuel
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700 1 _ |a Ashok Kumar Sreelatha, Ashwin
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700 1 _ |a Schulte, Claudia
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700 1 _ |a Grover, Sandeep
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700 1 _ |a Portugal, Berta
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700 1 _ |a Lee, Pei-Chen
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700 1 _ |a May, Patrick
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700 1 _ |a Bobbili, Dheeraj
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700 1 _ |a Lichtner, Peter
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700 1 _ |a Singleton, Andrew B
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700 1 _ |a Mellick, George D
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700 1 _ |a Zimprich, Alexander A
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700 1 _ |a Rogaeva, Ekaterina A
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700 1 _ |a Lang, Anthony E
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700 1 _ |a Koks, Sulev
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700 1 _ |a Taba, Pille
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700 1 _ |a Lesage, Suzanne
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700 1 _ |a Brice, Alexis
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700 1 _ |a Corvol, Jean-Christophe
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700 1 _ |a Chartier-Harlin, Marie-Christine
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700 1 _ |a Mutez, Eugenie
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700 1 _ |a Brockmann, Kathrin
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700 1 _ |a Deutschlander, Angela B
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700 1 _ |a Hadjigeorgiou, Georgios M
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700 1 _ |a Dardiotis, Efthimios
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700 1 _ |a Stefanis, Leonidas
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700 1 _ |a Simitsi, Athina Maria
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700 1 _ |a Valente, Enza Maria
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700 1 _ |a Petrucci, Simona
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700 1 _ |a Straniero, Letizia
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700 1 _ |a Zecchinelli, Anna L
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700 1 _ |a Brighina, Laura
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700 1 _ |a Ferrarese, Carlo
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700 1 _ |a Annesi, Grazia
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700 1 _ |a Gagliardi, Monica
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700 1 _ |a Matsuo, Hirotaka
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700 1 _ |a Nakayama, Akiyoshi
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700 1 _ |a Hattori, Nobutaka
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700 1 _ |a Nishioka, Kenya
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700 1 _ |a Chung, Sun Ju
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700 1 _ |a Kim, Yun Joong
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700 1 _ |a Kolber, Pierre
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700 1 _ |a Van De Warrenburg, Bart P C
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700 1 _ |a Bloem, Bastiaan R
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700 1 _ |a Toft, Mathias
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700 1 _ |a Pihlstrøm, Lasse
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700 1 _ |a Correia Guedes, Leonor
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700 1 _ |a Ferreira, Joaquim J
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700 1 _ |a Bardien, Soraya
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700 1 _ |a Carr, Jonathan
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700 1 _ |a Tolosa, Eduardo
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700 1 _ |a Ezquerra, Mario
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700 1 _ |a Pastor, Pau
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700 1 _ |a Diez-Fairen, Monica
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700 1 _ |a Wirdefeldt, Karin
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700 1 _ |a Pedersen, Nancy L
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700 1 _ |a Ran, Caroline
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700 1 _ |a Belin, Andrea C
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700 1 _ |a Puschmann, Andreas
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700 1 _ |a Hellberg, Clara
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700 1 _ |a Morrison, Karen E
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700 1 _ |a Tan, Manuela M
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700 1 _ |a Krainc, Dimitri
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700 1 _ |a Burbulla, Lena F.
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700 1 _ |a Farrer, Matthew
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700 1 _ |a Krüger, Rejko
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700 1 _ |a Elbaz, Alexis
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700 1 _ |a Genetics, Comprehensive Unbiased Risk Factor Assessment for
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700 1 _ |a Disease, Environment in Parkinson's
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773 _ _ |a 10.1212/WNL.0000000000209620
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