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@ARTICLE{Dogan:201200,
      author       = {Dogan, I. and Sass, C. and Mirzazade, S. and Kleiman, A.
                      and Werner, C. J. and Pohl, A. and Schiefer, J. and
                      Binkofski, F. and Schulz, J. B. and Shah, N. J. and Reetz,
                      K.},
      title        = {{N}eural correlates of impaired emotion processing in
                      manifest {H}untington's disease},
      journal      = {Social cognitive and affective neuroscience},
      volume       = {9},
      number       = {5},
      issn         = {1749-5024},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {FZJ-2015-03505},
      pages        = {671 - 680},
      year         = {2014},
      abstract     = {The complex phenotype of Huntington’s disease (HD)
                      encompasses motor, psychiatric and cognitive dysfunctions,
                      including early impairments in emotion recognition. In this
                      first functional magnetic resonance imaging study, we
                      investigated emotion-processing deficits in 14 manifest HD
                      patients and matched controls. An emotion recognition task
                      comprised short video clips displaying one of six basic
                      facial expressions (sadness, happiness, disgust, fear, anger
                      and neutral). Structural changes between patients and
                      controls were assessed by means of voxel-based morphometry.
                      Along with deficient recognition of negative emotions,
                      patients exhibited predominantly lower neural response to
                      stimuli of negative valences in the amygdala, hippocampus,
                      striatum, insula, cingulate and prefrontal cortices, as well
                      as in sensorimotor, temporal and visual areas. Most of the
                      observed reduced activity patterns could not be explained
                      merely by regional volume loss. Reduced activity in the
                      thalamus during fear correlated with lower thalamic volumes.
                      During the processing of sadness, patients exhibited
                      enhanced amygdala and hippocampal activity along with
                      reduced recruitment of the medial prefrontal cortex. Higher
                      amygdala activity was related to more pronounced amygdala
                      atrophy and disease burden. Overall, the observed
                      emotion-related dysfunctions in the context of structural
                      neurodegeneration suggest both disruptions of
                      striatal-thalamo-cortical loops and potential compensation
                      mechanism with greater disease severity in manifest HD.},
      cin          = {INM-4 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-4-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {332 - Imaging the Living Brain (POF2-332)},
      pid          = {G:(DE-HGF)POF2-332},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000336489000014},
      pubmed       = {pmid:23482620},
      doi          = {10.1093/scan/nst029},
      url          = {https://juser.fz-juelich.de/record/201200},
}