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@ARTICLE{Pelzer:873615,
      author       = {Pelzer, Esther A. and Dillenburger, Barbara and Grundmann,
                      Sophie and Iliaev, Vladimir and Aschenberg, Sophie and
                      Melzer, Corina and Hess, Martin and Fink, Gereon R. and
                      Eggers, Carsten and Tittgemeyer, Marc and Timmermann, Lars},
      title        = {{H}ypomania and saccadic changes in {P}arkinson’s
                      disease: influence of {D}2 and {D}3 dopaminergic signalling},
      journal      = {npj Parkinson's Disease},
      volume       = {6},
      number       = {1},
      issn         = {2373-8057},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {FZJ-2020-00858},
      pages        = {5},
      year         = {2020},
      abstract     = {In order to understand the influence of two dopaminergic
                      signalling pathways, TaqIA rs1800497 (influencing striatal
                      D2 receptor density) and Ser9Gly rs6280 (influencing the
                      striatal D3 dopamine-binding affinity), on saccade
                      generation and psychiatric comorbidities in Parkinson’s
                      disease, this study aimed to investigate the association of
                      saccadic performance in hypomanic or impulsive behaviour in
                      parkinsonian patients; besides we questioned whether
                      variants of D2 (A1+/A1−) and D3 (B1+/B1−) receptor
                      polymorphism influence saccadic parameters differently, and
                      if clinical parameters or brain connectivity changes
                      modulate this association in the nigro-caudatal and
                      nigro-collicular tract. Initially, patients and controls
                      were compared regarding saccadic performance and differed in
                      the parameter duration in memory-guided saccades (MGS) and
                      visually guided saccades (VGS) trials (p < 0.0001) and
                      in the MGS trial (p < 0.03). We were able to find
                      associations between hypomanic behaviour (HPS) and saccade
                      parameters (duration, latency, gain and amplitude) for both
                      conditions [MGS (p = 0.036); VGS (p = 0.033)], but
                      not for impulsive behaviour. For the A1 variant duration was
                      significantly associated with HPS [VGS (p = 0.024); MGS
                      (p = 0.033)]. In patients with the B1 variant, HPS
                      scores were more consistently associated with duration [VGS
                      (p = 0.005); MGS (p = 0.015), latency [VGS
                      (p = 0.022)]] and amplitude [MGS (p = 0.006); VGS
                      (p = 0.005)]. The mediation analysis only revealed a
                      significant indirect effect for amplitude in the MGS
                      modality for the variable UPDRS-ON (p < 0.05). All other
                      clinical scales and brain connectivity parameters were not
                      associated with behavioural traits. Collectively, our
                      findings stress the role of striatal D2 and D3 signalling
                      mechanisms in saccade generation and suggest that saccadic
                      performance is associated with the clinical psychiatric
                      state in Parkinson’s disease.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31970287},
      UT           = {WOS:000510945800001},
      doi          = {10.1038/s41531-019-0107-3},
      url          = {https://juser.fz-juelich.de/record/873615},
}