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@ARTICLE{Domenighetti:270631,
      author       = {Domenighetti, Cloé and Sugier, Pierre-Emmanuel and Ashok
                      Kumar Sreelatha, Ashwin and Schulte, Claudia and Grover,
                      Sandeep and Portugal, Berta and Lee, Pei-Chen and May,
                      Patrick and Bobbili, Dheeraj and Radivojkov Blagojevic,
                      Milena and Lichtner, Peter and Singleton, Andrew B and
                      Hernandez, Dena and Edsall, Connor and Mellick, George D and
                      Zimprich, Alexander A and Pirker, Walter and Rogaeva,
                      Ekaterina A and Lang, Anthony E and Koks, Sulev and Taba,
                      Pille and Lesage, Suzanne and Brice, Alexis and Corvol,
                      Jean-Christophe and Chartier-Harlin, Marie-Christine and
                      Mutez, Eugenie and Brockmann, Kathrin and Deutschlander,
                      Angela B and Hadjigeorgiou, Georgios M and Dardiotis,
                      Efthimios and Stefanis, Leonidas and Simitsi, Athina Maria
                      and Valente, Enza Maria and Petrucci, Simona and Straniero,
                      Letizia and Zecchinelli, Anna L and Pezzoli, Gianni and
                      Brighina, Laura and Ferrarese, Carlo and Annesi, Grazia and
                      Quattrone, Andrea and Gagliardi, Monica and Matsuo, Hirotaka
                      and Nakayama, Akiyoshi and Hattori, Nobutaka and Nishioka,
                      Kenya and Chung, Sun Ju and Kim, Yun Joong and Kolber,
                      Pierre and Van De Warrenburg, Bart P C and Bloem, Bastiaan R
                      and Toft, Mathias and Pihlstrøm, Lasse and Correia Guedes,
                      Leonor and Ferreira, Joaquim J and Bardien, Soraya and Carr,
                      Jonathan and Tolosa, Eduardo and Ezquerra, Mario and Pastor,
                      Pau and Diez-Fairen, Monica and Wirdefeldt, Karin and
                      Pedersen, Nancy L and Ran, Caroline and Belin, Andrea C and
                      Puschmann, Andreas and Hellberg, Clara and Clarke, Carl E
                      and Morrison, Karen E and Tan, Manuela M and Krainc, Dimitri
                      and Burbulla, Lena F. and Farrer, Matthew and Krüger, Rejko
                      and Gasser, Thomas and Sharma, Manu and Elbaz, Alexis and
                      Genetics, Comprehensive Unbiased Risk Factor Assessment for},
      collaboration = {Disease, Environment in Parkinson's},
      title        = {{A}ssociation of {B}ody {M}ass {I}ndex and {P}arkinson
                      {D}isease: {A} {B}idirectional {M}endelian {R}andomization
                      {S}tudy.},
      journal      = {Neurology},
      volume       = {103},
      number       = {3},
      issn         = {0028-3878},
      address      = {[Erscheinungsort nicht ermittelbar]},
      publisher    = {Ovid},
      reportid     = {DZNE-2024-00803},
      pages        = {e209620},
      year         = {2024},
      abstract     = {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.},
      keywords     = {Humans / Mendelian Randomization Analysis / Parkinson
                      Disease: genetics / Parkinson Disease: epidemiology / Body
                      Mass Index / Polymorphism, Single Nucleotide: genetics /
                      Female / Male / Genome-Wide Association Study / Middle Aged
                      / Aged / Risk Factors},
      cin          = {AG Gasser / AG Burbulla},
      ddc          = {610},
      cid          = {I:(DE-2719)1210000 / I:(DE-2719)5000074},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38986057},
      doi          = {10.1212/WNL.0000000000209620},
      url          = {https://pub.dzne.de/record/270631},
}