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@ARTICLE{Meinhardt:904392,
      author       = {Meinhardt, Marcus W. and Pfarr, Simone and Fouquet,
                      Grégory and Rohleder, Cathrin and Meinhardt, Manuela L. and
                      Barroso-Flores, Janet and Hoffmann, Rebecca and Jeanblanc,
                      Jérôme and Paul, Elisabeth and Wagner, Konstantin and
                      Hansson, Anita C. and Köhr, Georg and Meier, Nils and von
                      Bohlen und Halbach, Oliver and Bell, Richard L. and
                      Endepols, Heike and Neumaier, Bernd and Schönig, Kai and
                      Bartsch, Dusan and Naassila, Mickaël and Spanagel, Rainer
                      and Sommer, Wolfgang H.},
      title        = {{P}silocybin targets a common molecular mechanism for
                      cognitive impairment and increased craving in alcoholism},
      journal      = {Science advances},
      volume       = {7},
      number       = {47},
      issn         = {2375-2548},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {FZJ-2021-05962},
      pages        = {eabh2399},
      year         = {2021},
      abstract     = {Alcohol-dependent patients commonly show impairments in
                      executive functions that facilitate craving and can lead to
                      relapse. However, the molecular mechanisms leading to
                      executive dysfunction in alcoholism are poorly understood,
                      and new effective pharmacological treatments are desired.
                      Here, using a bidirectional neuromodulation approach, we
                      demonstrate a causal link between reduced prefrontal mGluR2
                      function and both impaired executive control and alcohol
                      craving. A neuron-specific prefrontal mGluR2 knockdown in
                      rats generated a phenotype of reduced cognitive flexibility
                      and excessive alcohol seeking. Conversely, virally restoring
                      prefrontal mGluR2 levels in alcohol-dependent rats rescued
                      these pathological behaviors. In the search for a
                      pharmacological intervention with high translational
                      potential, psilocybin was capable of restoring mGluR2
                      expression and reducing relapse behavior. Last, we propose a
                      FDG-PET biomarker strategy to identify mGluR2
                      treatment-responsive individuals. In conclusion, we
                      identified a common molecular pathological mechanism for
                      both executive dysfunction and alcohol craving and provided
                      a personalized mGluR2 mechanism-based intervention strategy
                      for medication development for alcoholism.},
      cin          = {INM-5},
      ddc          = {500},
      cid          = {I:(DE-Juel1)INM-5-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34788104},
      UT           = {WOS:000720347400007},
      doi          = {10.1126/sciadv.abh2399},
      url          = {https://juser.fz-juelich.de/record/904392},
}