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@ARTICLE{Tscher:1028963,
      author       = {Tüscher, Oliver and Muthuraman, Muthuraman and Horstmann,
                      Johann-Philipp and Horta, Guilherme and Radyushkin,
                      Konstantin and Baumgart, Jan and Sigurdsson, Torfi and
                      Endle, Heiko and Ji, Haichao and Kuhnhäuser, Prisca and
                      Götz, Jan and Kepser, Lara-Jane and Lotze, Martin and
                      Grabe, Hans J. and Völzke, Henry and Leehr, Elisabeth J.
                      and Meinert, Susanne and Opel, Nils and Richers, Sebastian
                      and Stroh, Albrecht and Daun, Silvia and Tittgemeyer, Marc
                      and Uphaus, Timo and Steffen, Falk and Zipp, Frauke and
                      Groß, Joachim and Groppa, Sergiu and Dannlowski, Udo and
                      Nitsch, Robert and Vogt, Johannes},
      title        = {{A}ltered cortical synaptic lipid signaling leads to
                      intermediate phenotypes of mental disorders},
      journal      = {Molecular psychiatry},
      volume       = {29},
      number       = {11},
      issn         = {1359-4184},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {FZJ-2024-04900},
      pages        = {3537 - 3552},
      year         = {2024},
      abstract     = {Excitation/inhibition (E/I) balance plays important roles
                      in mental disorders. Bioactive phospholipids like
                      lysophosphatidic acid (LPA) are synthesized by the enzyme
                      autotaxin (ATX) at cortical synapses and modulate
                      glutamatergic transmission, and eventually alter E/I balance
                      of cortical networks. Here, we analyzed functional
                      consequences of altered E/I balance in 25 human subjects
                      induced by genetic disruption of the synaptic lipid
                      signaling modifier PRG-1, which were compared to 25 age and
                      sex matched control subjects. Furthermore, we tested
                      therapeutic options targeting ATX in a related mouse line.
                      Using EEG combined with TMS in an instructed fear paradigm,
                      neuropsychological analysis and an fMRI based episodic
                      memory task, we found intermediate phenotypes of mental
                      disorders in human carriers of a loss-of-function single
                      nucleotide polymorphism of PRG-1 (PRG-1R345T/WT).
                      Prg-1R346T/WT animals phenocopied human carriers showing
                      increased anxiety, a depressive phenotype and lower stress
                      resilience. Network analysis revealed that coherence and
                      phase-amplitude coupling were altered by PRG-1 deficiency in
                      memory related circuits in humans and mice alike. Brain
                      oscillation phenotypes were restored by inhibtion of ATX in
                      Prg-1 deficient mice indicating an interventional potential
                      for mental disorders.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525) / DFG project G:(GEPRIS)431549029 - SFB 1451:
                      Schlüsselmechanismen normaler und krankheitsbedingt
                      gestörter motorischer Kontrolle (431549029)},
      pid          = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {38806692},
      UT           = {WOS:001234275100002},
      doi          = {10.1038/s41380-024-02598-2},
      url          = {https://juser.fz-juelich.de/record/1028963},
}