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@ARTICLE{Mhleisen:841704,
      author       = {Mühleisen, Thomas and Reinbold, Céline S and Forstner,
                      Andreas J and Abramova, Lilia I and Alda, Martin and
                      Babadjanova, Gulja and Bauer, Michael and Brennan, Paul and
                      Chuchalin, Alexander and Cruceanu, Cristiana and Czerski,
                      Piotr M and Degenhardt, Franziska and Fischer, Sascha B and
                      Fullerton, Janice M and Gordon, Scott D and
                      Grigoroiu-Serbanescu, Maria and Grof, Paul and Hauser,
                      Joanna and Hautzinger, Martin and Herms, Stefan and
                      Hoffmann, Per and Kammerer-Ciernioch, Jutta and
                      Khusnutdinova, Elza and Kogevinas, Manolis and Krasnov,
                      Valery and Lacour, André and Laprise, Catherine and Leber,
                      Markus and Lissowska, Jolanta and Lucae, Susanne and Maaser,
                      Anna and Maier, Wolfgang and Martin, Nicholas G and
                      Mattheisen, Manuel and Mayoral, Fermin and McKay, James D
                      and Medland, Sarah E and Mitchell, Philip B and Moebus,
                      Susanne and Montgomery, Grant W and Müller-Myhsok, Bertram
                      and Oruc, Lilijana and Pantelejeva, Galina and Pfennig,
                      Andrea and Pojskic, Lejla and Polonikov, Alexey and Reif,
                      Andreas and Rivas, Fabio and Rouleau, Guy A and Schenk,
                      Lorena M and Schofield, Peter R and Schwarz, Markus and
                      Streit, Fabian and Strohmaier, Jana and Szeszenia-Dabrowska,
                      Neonila and Tiganov, Alexander S and Treutlein, Jens and
                      Turecki, Gustavo and Vedder, Helmut and Witt, Stephanie H
                      and Schulze, Thomas G and Rietschel, Marcella and Nöthen,
                      Markus M and Cichon, Sven},
      title        = {{G}ene set enrichment analysis and expression pattern
                      exploration implicate an involvement of neurodevelopmental
                      processes in bipolar disorder},
      journal      = {Journal of affective disorders},
      volume       = {228},
      issn         = {0165-0327},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2018-00012},
      pages        = {20-25},
      year         = {2018},
      abstract     = {Bipolar disorder (BD) is a common and highly heritable
                      disorder of mood. Genome-wide association studies (GWAS)
                      have identified several independent susceptibility loci. In
                      order to extract more biological information from GWAS data,
                      multi-locus approaches represent powerful tools since they
                      utilize knowledge about biological processes to integrate
                      functional sets of genes at strongly to moderately
                      associated loci.We conducted gene set enrichment analyses
                      (GSEA) using 2.3 million single-nucleotide polymorphisms,
                      397 Reactome pathways and 24,025 patients with BD and
                      controls. RNA expression of implicated individual genes and
                      gene sets were examined in post-mortem brains across
                      lifespan.Two pathways showed a significant enrichment after
                      correction for multiple comparisons in the GSEA: GRB2 events
                      in ERBB2 signaling, for which 6 of 21 genes were BD
                      associated (PFDR = 0.0377), and NCAM signaling for neurite
                      out-growth, for which 11 out of 62 genes were BD associated
                      (PFDR = 0.0451). Most pathway genes showed peaks of RNA
                      co-expression during fetal development and infancy and
                      mapped to neocortical areas and parts of the limbic
                      system.Pathway associations were technically reproduced by
                      two methods, although they were not formally replicated in
                      independent samples. Gene expression was explored in
                      controls but not in patients.Pathway analysis in large GWAS
                      data of BD and follow-up of gene expression patterns in
                      healthy brains provide support for an involvement of
                      neurodevelopmental processes in the etiology of this
                      neuropsychiatric disease. Future studies are required to
                      further evaluate the relevance of the implicated genes on
                      pathway functioning and clinical aspects of BD.},
      cin          = {INM-1},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-1-20090406},
      pnm          = {571 - Connectivity and Activity (POF3-571)},
      pid          = {G:(DE-HGF)POF3-571},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29197740},
      UT           = {WOS:000424331400003},
      doi          = {10.1016/j.jad.2017.11.068},
      url          = {https://juser.fz-juelich.de/record/841704},
}