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@ARTICLE{Winterer:202035,
      author       = {Winterer, Georg and Gallinat, Jürgen and Brinkmeyer,
                      Jürgen and Musso, Francesco and Kornhuber, Johannes and
                      Thuerauf, Norbert and Rujescu, Dan and Favis, Reyna and Sun,
                      Yu and Franc, Monique A. and Ouwerkerk-Mahadevan, Sivi and
                      Janssens, Luc and Timmers, Maarten and Streffer, Johannes
                      R.},
      title        = {{A}llosteric alpha-7 nicotinic receptor modulation and
                      {P}50 sensory gating in schizophrenia: {A}
                      proof-of-mechanism study},
      journal      = {Neuropharmacology},
      volume       = {64},
      issn         = {0028-3908},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2015-04324},
      pages        = {197 - 204},
      year         = {2013},
      abstract     = {In this multicenter, double-blind, placebo-controlled,
                      randomized, four way cross-over proof-of-mechanism study, we
                      tested the effect of the positive allosteric α7 nicotinic
                      acetylcholine receptor (nAChR) modulator JNJ-39393406 in a
                      key translational assay (sensory P50 gating) in 39 regularly
                      smoking male patients with schizophrenia. All patients were
                      clinically stable and JNJ-39393406 was administered as an
                      adjunct treatment to antipsychotics. No indication was found
                      that JNJ-39393406 has the potential to reverse basic
                      deficits of information processing in schizophrenia (sensory
                      P50 gating) or has a significant effect on other tested
                      electrophysiological markers (MMN, P300 and quantitative
                      resting EEG). Sensitivity analyses including severity of
                      disease, baseline P50 gating, medication and gene variants
                      of the CHRNA7 gene did not reveal any subgroups with
                      consistent significant effects. It is discussed that
                      potential positive effects in subgroups not present or not
                      large enough in the current study or upon chronic dosing are
                      possible, but unlikely to be developed.},
      cin          = {INM-3 / INM-4},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-4-20090406},
      pnm          = {333 - Pathophysiological Mechanisms of Neurological and
                      Psychiatric Diseases (POF2-333)},
      pid          = {G:(DE-HGF)POF2-333},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000311250300023},
      pubmed       = {pmid:22766391},
      doi          = {10.1016/j.neuropharm.2012.06.040},
      url          = {https://juser.fz-juelich.de/record/202035},
}