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@ARTICLE{Gandal:201866,
      author       = {Gandal, Michael J. and Edgar, J. Christopher and Klook,
                      Kerstin and Siegel, Steven J.},
      title        = {{G}amma synchrony: {T}owards a translational biomarker for
                      the treatment-resistant symptoms of schizophrenia},
      journal      = {Neuropharmacology},
      volume       = {62},
      number       = {3},
      issn         = {0028-3908},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2015-04160},
      pages        = {1504 - 1518},
      year         = {2012},
      abstract     = {The lack of efficacy for antipsychotics with respect to
                      negative symptoms and cognitive deficits is a significant
                      obstacle for the treatment of schizophrenia. Developing new
                      drugs to target these symptoms requires appropriate neural
                      biomarkers that can be investigated in model organisms, be
                      used to track treatment response, and provide insight into
                      pathophysiological disease mechanisms. A growing body of
                      evidence indicates that neural oscillations in the gamma
                      frequency range (30–80 Hz) are disturbed in schizophrenia.
                      Gamma synchrony has been shown to mediate a host of sensory
                      and cognitive functions, including perceptual encoding,
                      selective attention, salience, and working memory –
                      neurocognitive processes that are dysfunctional in
                      schizophrenia and largely refractory to treatment. This
                      review summarizes the current state of clinical literature
                      with respect to gamma-band responses (GBRs) in
                      schizophrenia, focusing on resting and auditory paradigms.
                      Next, preclinical studies of schizophrenia that have
                      investigated gamma-band activity are reviewed to gain
                      insight into neural mechanisms associated with these
                      deficits. We conclude that abnormalities in gamma synchrony
                      are ubiquitous in schizophrenia and likely reflect an
                      elevation in baseline cortical gamma synchrony (‘noise’)
                      coupled with reduced stimulus-evoked GBRs (‘signal’).
                      Such a model likely reflects hippocampal and cortical
                      dysfunction, as well as reduced glutamatergic signaling with
                      downstream GABAergic deficits, but is probably less
                      influenced by dopaminergic abnormalities implicated in
                      schizophrenia. Finally, we propose that analogous
                      signal-to-noise deficits in the flow of cortical information
                      in preclinical models are useful targets for the development
                      of new drugs that target the treatment-resistant symptoms of
                      schizophrenia.},
      cin          = {INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {331 - Signalling Pathways and Mechanisms in the Nervous
                      System (POF2-331)},
      pid          = {G:(DE-HGF)POF2-331},
      typ          = {PUB:(DE-HGF)16 / PUB:(DE-HGF)36},
      UT           = {WOS:000300533800034},
      pubmed       = {pmid:21349276},
      doi          = {10.1016/j.neuropharm.2011.02.007},
      url          = {https://juser.fz-juelich.de/record/201866},
}