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@ARTICLE{Thimm:16837,
      author       = {Thimm, M. and Kircher, T. and Kellermann, T. and Markov, V.
                      and Krach, S. and Jansen, A. and Zerres, K. and Eggermann,
                      T. and Stöcker, T. and Shah, N.J. and Nöthen, M.M. and
                      Rietschel, M. and Witt, S.H. and Mathiak, K. and Krug, A.},
      title        = {{E}ffects of a {CACNA}1{C} genotype on attention networks
                      in healthy individuals.},
      journal      = {Psychological medicine},
      volume       = {41},
      issn         = {0033-2917},
      address      = {Cambridge},
      publisher    = {Cambridge Univ. Press},
      reportid     = {PreJuSER-16837},
      pages        = {1551 - 1561},
      year         = {2011},
      note         = {This work was supported by the Federal Ministry of
                      Education and Research (BMBF; Brain Imaging Centre West,
                      01GO0204 and 01GW0751) and by the START Program of the
                      Medical Faculty of RWTH Aachen University.},
      abstract     = {Recent genetic studies found the A allele of the variant
                      rs1006737 in the alpha 1C subunit of the L-type
                      voltage-gated calcium channel (CACNA1C) gene to be
                      over-represented in patients with psychosis, including
                      schizophrenia, bipolar disorder and major depressive
                      disorder. In these disorders, attention deficits are among
                      the main cognitive symptoms and have been related to altered
                      neural activity in cerebral attention networks. The
                      particular effect of CACNA1C on neural function, such as
                      attention networks, remains to be elucidated.The current
                      event-related functional magnetic resonance imaging (fMRI)
                      study investigated the effect of the CACNA1C gene on brain
                      activity in 80 subjects while performing a scanner-adapted
                      version of the Attention Network Test (ANT). Three domains
                      of attention were probed simultaneously: alerting, orienting
                      and executive control of attention.Risk allele carriers
                      showed impaired performance in alerting and orienting in
                      addition to reduced neural activity in the right inferior
                      parietal lobule [Brodmann area (BA) 40] during orienting and
                      in the medial frontal gyrus (BA 8) during executive control
                      of attention. These areas belong to networks that have been
                      related to impaired orienting and executive control
                      mechanisms in neuropsychiatric disorders.Our results suggest
                      that CACNA1C plays a role in the development of specific
                      attention deficits in psychiatric disorders by modulation of
                      neural attention networks.},
      keywords     = {Adolescent / Adult / Attention: physiology / Brain:
                      physiology / Calcium Channels, L-Type: genetics / Cues /
                      Female / Genotype / Humans / Image Processing,
                      Computer-Assisted / Magnetic Resonance Imaging: methods /
                      Male / Middle Aged / Polymorphism, Single Nucleotide:
                      genetics / Reaction Time / Reference Values / Task
                      Performance and Analysis / Young Adult / CACNA1C protein,
                      human (NLM Chemicals) / Calcium Channels, L-Type (NLM
                      Chemicals) / J (WoSType)},
      cin          = {INM-4 / INM-1 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-4-20090406 / I:(DE-Juel1)INM-1-20090406 /
                      I:(DE-Juel1)INM-5-20090406},
      pnm          = {Neurowissenschaften (FUEK255) / 333 - Pathophysiological
                      Mechanisms of Neurological and Psychiatric Diseases
                      (POF2-333)},
      pid          = {G:(DE-Juel1)FUEK255 / G:(DE-HGF)POF2-333},
      shelfmark    = {Psychology, Clinical / Psychiatry / Psychology},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21078228},
      UT           = {WOS:000291854700022},
      doi          = {10.1017/S0033291710002217},
      url          = {https://juser.fz-juelich.de/record/16837},
}