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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},
}