% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Kabaoglu:285741,
      author       = {Kabaoglu, Burce and Garulli, Elisa L and De Sa, Rafael and
                      Vogt, Arend and Behrsing, Ruben and Skrobot, Matej and
                      Paulat, Raik and Pollak, Patrick and Guldin, Lynn S and
                      Gerster, Moritz and Neumann, Wolf-Julian and Endres,
                      Matthias and Harms, Christoph and Wenger, Nikolaus},
      title        = {{S}hift in motor-state equilibrium explains gait therapy
                      effects of apomorphine in experimental {P}arkinsonism.},
      journal      = {Experimental neurology},
      volume       = {401},
      issn         = {0014-4886},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2026-00298},
      pages        = {115704},
      year         = {2026},
      abstract     = {Gait impairments remain a major therapeutic challenge in
                      Parkinson's disease (PD). Apomorphine is gaining renewed
                      clinical attention with the expanding use of pump infusion
                      systems. Yet the specific role of apomorphine on the neural
                      regulation of gait has remained poorly characterized,
                      limiting its targeted use for symptom-specific therapy in
                      PD. Here, we examined the neurobehavioral effects of
                      apomorphine on runway locomotion in the unilateral
                      6-hydroxydopamine (6-OHDA) rat model. Therapeutic drug doses
                      significantly increased total walking distance, related to
                      reduced akinesia and prolonged gait episodes. Conversely, 3D
                      kinematic analysis revealed reduced limb velocities under
                      medication. At the neural level, therapy doses selectively
                      enhanced cortical high-gamma rhythms without substantially
                      altering beta or low-gamma activity. Instead, beta and
                      low-gamma oscillations were consistently suppressed during
                      motor activity in both medication ON and OFF conditions.
                      Neurobehavioral correlations showed that transitions into
                      gait were facilitated by reductions in beta and low-gamma
                      activity, whereas transitions to akinesia were primarily
                      suppressed when high-gamma activity was elevated. Our
                      findings highlight that cortical oscillations can serve as
                      state specific biomarkers for gait impairments in PD. We
                      further propose that the complex therapy effects of
                      apomorphine are best explained by a shift in motor-state
                      equilibrium that is defined by the transitions of akinesia,
                      stationary movements and gait. Together, these insights
                      establish a mechanistic framework to guide the development
                      of targeted gait therapies in PD.},
      keywords     = {Gait therapy (Other) / Motor control (Other) / Neural
                      oscillations (Other) / Parkinson's disease (Other)},
      cin          = {AG Endres},
      ddc          = {610},
      cid          = {I:(DE-2719)1811005},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41765318},
      doi          = {10.1016/j.expneurol.2026.115704},
      url          = {https://pub.dzne.de/record/285741},
}