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@ARTICLE{Blaschke:1050467,
      author       = {Blaschke, Stefan J. and Backes, Heiko and Vlachakis, Susan
                      and Rautenberg, Nora and Demir, Seda and Wiedermann, Dirk
                      and Aswendt, Markus and Fink, Gereon R. and Schroeter,
                      Michael and Rueger, Maria A.},
      title        = {{S}ubacute cathodal transcranial direct current stimulation
                      rescues secondary thalamic neurodegeneration after cortical
                      stroke in mice},
      journal      = {Experimental neurology},
      volume       = {398},
      issn         = {0014-4886},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2026-00236},
      pages        = {115604 -},
      year         = {2026},
      abstract     = {Transcranial direct current stimulation (tDCS) is a
                      clinically promising neuromodulatory therapy, capable of
                      promoting function and motor recovery after stroke. Beyond
                      the primary stroke lesion, remote networks disturbances,
                      e.g., stroke-induced secondary neurodegeneration (SND), are
                      related to long-term disabilities. Under the hypothesis that
                      tDCS promotes recovery by supporting neuroprotection, we
                      investigated the effects of tDCS on thalamic SND after
                      stroke. Three days after cortical stroke, induced by
                      photothrombosis, cathodal tDCS over the lesioned cortex was
                      performed daily for ten days (39.6 kC/m2). SND, i.e.,
                      neuronal loss, and inflammation in the ipsilesional thalamus
                      were evaluated ex vivo 28 days after stroke. Parameters of
                      functional thalamic network integration measured by
                      resting-state functional magnetic resonance imaging
                      (rs-fMRI) were conducted longitudinally. To assess the
                      effects of tDCS on glucose metabolism, positron emission
                      tomography (PET) was performed after a similar tDCS regimen
                      in healthy mice. Repetitive tDCS decreased the ipsilateral
                      thalamic glucose metabolism in unlesioned animals. Four
                      weeks after cortical stroke, secondary glial scaring was
                      found in the ipsilesional thalamus, its extent correlating
                      to the cortical lesion size (R2 = 0.54, p < 0.001). Notably,
                      while it did not affect glial scaring, tDCS reduced thalamic
                      neurodegeneration by over 60 $\%$ (p < 0.05), being
                      reflected by parameters of functional thalamic integration
                      as assessed by rs-fMRI. Additionally, tDCS downregulated the
                      pro-inflammatory polarization of microglia. Overall, tDCS
                      ameliorated the stroke-induced remote SND, in parallel to
                      mitigating sustained neuroinflammation. Thus, the data show
                      that tDCS exerts previously unknown effects on remote brain
                      regions after stroke.Keywords: Experimental stroke; Glucose
                      metabolism; Neuroinflammation; Secondary neurodegeneration;
                      Stroke recovery; Transcranial direct current stimulation.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5252},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1016/j.expneurol.2025.115604},
      url          = {https://juser.fz-juelich.de/record/1050467},
}