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@ARTICLE{Sosero:272822,
      author       = {Sosero, Yuri L and Bandres-Ciga, Sara and Ferwerda, Bart
                      and Tocino, Maria T P and Belloso, Dìaz R and Gómez-Garre,
                      Pilar and Faouzi, Johann and Taba, Pille and Pavelka, Lukas
                      and Marques, Tainà M and Gomes, Clarissa P C and Kolodkin,
                      Alexey and May, Patrick and Milanowski, Lukasz M and
                      Wszolek, Zbigniew K and Uitti, Ryan J and Heutink, Peter and
                      van Hilten, Jacobus J and Simon, David K and Eberly, Shirley
                      and Alvarez, Ignacio and Krohn, Lynne and Yu, Eric and
                      Freeman, Kathryn and Rudakou, Uladzislau and Ruskey,
                      Jennifer A and Asayesh, Farnaz and Menéndez-Gonzàlez,
                      Manuel and Pastor, Pau and Ross, Owen A and Krüger, Rejko
                      and Corvol, Jean-Christophe and Koks, Sulev and Mir, Pablo
                      and De Bie, Rob M A and Iwaki, Hirotaka and Gan-Or, Ziv},
      collaboration = {Consortium, NCER-PD and Consortium, International
                      Parkinson's Disease Genomic},
      othercontributors = {Acharya, Geeta and Aguayo, Gloria and Alexandre, Myriam and
                          Ali, Muhammad and Ammerlann, Wim and Arena, Giuseppe and
                          Balling, Rudi and Bassis, Michele and Beaumont, Katy and
                          Becker, Regina and Bellora, Camille and Berchem, Guy and
                          Berg, Daniela and Bisdorff, Alexandre and Boussaad, Ibrahim
                          and Brockmann, Kathrin and Calme, Jessica and Castillo,
                          Lorieza and Contesotto, Gessica and Diederich, Nico and
                          Dondelinger, Rene and Esteves, Daniela and Fagherazzi, Guy
                          and Ferrand, Jean-Yves and Gantenbein, Manon and Gasser,
                          Thomas and Gawron, Piotr and Ghosh, Soumyabrata and
                          Giraitis, Marijus and Glaab, Enrico and De Lope, Elisa
                          Gómez and Graas, Jérôme and Graziano, Mariella and
                          Groues, Valentin and Grünewald, Anne and Gu, Wei and
                          Hammot, Gaël and Hanff, Anne-Marie and Hansen, Linda and
                          Heneka, Michael and Henr, Estelle and Herbrink, Sylvia and
                          Herzinger, Sascha and Heymann, Michael and Hu, Michele and
                          Hundt, Alexander and Jacoby, Nadine and Lebioda, Jacek
                          Jaroslaw and Jaroz, Yohan and Jónsdóttir, Sonja and
                          Klopfenstein, Quentin and Klucken, Jochen and Krüger, Rejko
                          and Lambert, Pauline and Landoulsi, Zied and Lentz, Roseline
                          and Liepelt-Scarfone, Inga and Liszka, Robert and Longhino,
                          Laura and Lorentz, Victoria and Lupu, Paula Cristina and
                          Marques, Tainá M and Mackay, Clare and Maetzler, Walter and
                          Marcus, Katrin and Marques, Guilherme and Conde, Patricia
                          Martins and May, Patrick and Mcintyre, Deborah and Mediouni,
                          Chouaib and Meisch, Francoise and Menster, Myriam and
                          Minelli, Maura and Mittelbronn, Michel and Mollenhauer, Brit
                          and Mühlschlegel, Friedrich and Nati, Romain and Nehrbass,
                          Ulf and Nickels, Sarah and Nicolai, Beatrice and Nicolay,
                          Jean-Paul and Noor, Fozia and Ostaszewski, Marek and Gomes,
                          Clarissa P C and Pachchek, Sinthuja and Pauly, Claire and
                          Pauly, Laure and Pavelka, Lukas and Perquin, Magali and
                          Lima, Rosalina Ramos and Rauschenberger, Armin and Rawal,
                          Rajesh and Bobbili, Dheeraj Reddy and Roomp, Kirsten and
                          Rosales, Eduardo and Rosety, Isabel and Sandt, Estelle and
                          Sapienza, Stefano and Satagopam, Venkata and Schmitt,
                          Margaux and Schmitz, Sabine and Schneide, Reinhard and
                          Schwamborn, Jens and Sharify, Amir and Soboleva, Ekaterina
                          and Sokolowska, Kate and Thien, Hermann and Thiry, Elodie
                          and Loo, Rebecca Ting Jiin and Trefois, Christophe and
                          Trouet, Johanna and Tsurkalenko, Olena and Vaillant, Michel
                          and Valenti, Mesele and Van Cutsem, Gilles and Vega, Carlos
                          and Boas, Liliana Vilas and Vyas, Maharshi and Wade-Martins,
                          Richard and Wilmes, Paul and Wollscheid-Lengeling, Evi and
                          Zelimkhanov, Gelani},
      title        = {{D}opamine {P}athway and {P}arkinson's {R}isk {V}ariants
                      {A}re {A}ssociated with {L}evodopa-{I}nduced {D}yskinesia.},
      journal      = {Movement disorders},
      volume       = {39},
      number       = {10},
      issn         = {0885-3185},
      address      = {New York, NY},
      publisher    = {Wiley},
      reportid     = {DZNE-2024-01240},
      pages        = {1773 - 1783},
      year         = {2024},
      abstract     = {Levodopa-induced dyskinesia (LID) is a common adverse
                      effect of levodopa, one of the main therapeutics used to
                      treat the motor symptoms of Parkinson's disease (PD).
                      Previous evidence suggests a connection between LID and a
                      disruption of the dopaminergic system as well as genes
                      implicated in PD, including GBA1 and LRRK2.Our goal was to
                      investigate the effects of genetic variants on risk and time
                      to LID.We performed a genome-wide association study (GWAS)
                      and analyses focused on GBA1 and LRRK2 variants. We also
                      calculated polygenic risk scores (PRS) including risk
                      variants for PD and variants in genes involved in the
                      dopaminergic transmission pathway. To test the influence of
                      genetics on LID risk we used logistic regression, and to
                      examine its impact on time to LID we performed Cox
                      regression including 1612 PD patients with and 3175 without
                      LID.We found that GBA1 variants were associated with LID
                      risk (odds ratio [OR] = 1.65; $95\%$ confidence interval
                      [CI], 1.21-2.26; P = 0.0017) and LRRK2 variants with reduced
                      time to LID onset (hazard ratio [HR] = 1.42; $95\%$ CI,
                      1.09-1.84; P = 0.0098). The fourth quartile of the PD PRS
                      was associated with increased LID risk $(ORfourth_quartile$
                      = 1.27; $95\%$ CI, 1.03-1.56; P = 0.0210). The third and
                      fourth dopamine pathway PRS quartiles were associated with a
                      reduced time to development of LID $(HRthird_quartile$ =
                      1.38; $95\%$ CI, 1.07-1.79; P = 0.0128; $HRfourth_quartile$
                      = 1.38; $95\%$ CI = 1.06-1.78; P = 0.0147).This study
                      suggests that variants implicated in PD and in the
                      dopaminergic transmission pathway play a role in the
                      risk/time to develop LID. Further studies will be necessary
                      to examine how these findings can inform clinical care. ©
                      2024 The Author(s). Movement Disorders published by Wiley
                      Periodicals LLC on behalf of International Parkinson and
                      Movement Disorder Society.},
      keywords     = {Humans / Levodopa: adverse effects / Parkinson Disease:
                      genetics / Parkinson Disease: drug therapy / Dyskinesia,
                      Drug-Induced: genetics / Male / Female / Aged / Leucine-Rich
                      Repeat Serine-Threonine Protein Kinase-2: genetics /
                      Glucosylceramidase: genetics / Middle Aged / Genome-Wide
                      Association Study / Dopamine: metabolism / Antiparkinson
                      Agents: adverse effects / Genetic Predisposition to Disease:
                      genetics / Polymorphism, Single Nucleotide: genetics / GBA1
                      (Other) / LRRK2 (Other) / Parkinson's disease (Other) /
                      dopamine (Other) / levodopa‐induced dyskinesia (Other) /
                      Levodopa (NLM Chemicals) / Leucine-Rich Repeat
                      Serine-Threonine Protein Kinase-2 (NLM Chemicals) /
                      Glucosylceramidase (NLM Chemicals) / LRRK2 protein, human
                      (NLM Chemicals) / Dopamine (NLM Chemicals) / GBA protein,
                      human (NLM Chemicals) / Antiparkinson Agents (NLM
                      Chemicals)},
      cin          = {AG Heutink},
      ddc          = {610},
      cid          = {I:(DE-2719)1210002},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11490412},
      pubmed       = {pmid:39132902},
      doi          = {10.1002/mds.29960},
      url          = {https://pub.dzne.de/record/272822},
}