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@ARTICLE{Kordys:842596,
      author       = {Kordys, Elena and Apetz, Nadine and Schneider, Katharina
                      and Duncan, Eilidh and Büschbell, Beatriz and Rohleder,
                      Cathrin and Sué, Michael and Drzezga, Alexander and
                      Neumaier, Bernd and Timmermann, Lars and Endepols},
      title        = {{M}otor impairment and compensation in a hemiparkinsonian
                      rat model: correlation between dopamine depletion severity,
                      cerebral metabolism and gait patterns},
      journal      = {EJNMMI Research},
      volume       = {7},
      number       = {1},
      issn         = {2191-219X},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {FZJ-2018-00809},
      pages        = {68},
      year         = {2017},
      abstract     = {BACKGROUND:In Parkinson's disease (PD), cerebral dopamine
                      depletion is associated with PD subtype-specific metabolic
                      patterns of hypo- and hypermetabolism. It has been
                      hypothesised that hypometabolism reflects impairment, while
                      hypermetabolism may indicate compensatory activity. In order
                      to associate metabolic patterns with pathophysiological and
                      compensatory mechanisms, we combined resting state
                      [18F]FDG-PET (to demonstrate brain metabolism in awake
                      animals), [18F]FDOPA-PET (dopamine depletion severity) and
                      gait analysis in a unilateral 6-hydroxydopamine rat
                      model.RESULTS:We found unilateral nigro-striatal
                      dopaminergic loss to decrease swing speed of the
                      contralesional forelimb and stride length of all paws in
                      association with depletion severity. Depletion severity was
                      found to correlate with compensatory changes such as
                      increased stance time of the other three paws and diagonal
                      weight shift to the ipsilesional hind paw. [18F]FDG-PET
                      revealed ipsilesional hypo- and contralesional
                      hypermetabolism; metabolic deactivation of the ipsilesional
                      network needed for sensorimotor integration
                      (hippocampus/retrosplenial cortex/lateral posterior
                      thalamus) was solely associated with bradykinesia, but
                      hypometabolism of the ipsilesional rostral forelimb area was
                      related to both pathological and compensatory gait changes.
                      Mixed effects were also found for hypermetabolism of the
                      contralesional midbrain locomotor region, while
                      contralesional striatal hyperactivation was linked to motor
                      impairments rather than compensation.CONCLUSIONS:Our results
                      indicate that ipsilesional hypo- and contralesional
                      hypermetabolism contribute to both motor impairment and
                      compensation. This is the first time when energy metabolism,
                      dopamine depletion and gait analysis were combined in a
                      hemiparkinsonian model. By experimentally increasing or
                      decreasing compensational brain activity, its potential and
                      limits can be further investigated.},
      cin          = {INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-5-20090406},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000408233100001},
      doi          = {10.1186/s13550-017-0317-9},
      url          = {https://juser.fz-juelich.de/record/842596},
}