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THE ROLE OF MAGNETIC STIMULATION IN BDNF-TARGETED THERAPY FOR SUBACUTE STROKE
Ji-Hye Kimand 4 co-authors
Chonnam National University Hospital
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-084
Presentation
Date TBA
Board: PS04-08PM-084
Event Information
Poster Board
PS04-08PM-084
Poster
View posterAbstract
Background: Brain-derived neurotrophic factor (BDNF) is a potent neurorestorative molecule, but its clinical translation is hindered by poor blood–brain barrier (BBB) penetration. Magnetic stimulation (MagStim) has been shown to transiently modulate BBB permeability without vascular damage. We investigated whether MagStim enhances BDNF delivery and confers synergistic neuroprotection in a rat model of ischemic stroke.
Methods: Transient middle cerebral artery occlusion (MCAO) was induced in rats. Fourteen days post-stroke, animals were assigned to four groups: Sham, MCAO Control, BDNF alone (intravenous), and MagStim+BDNF (MagStim immediately before intravenous BDNF). Infarct volume (TTC/MRI), neurological function (rotarod/NDS), and BDNF brain penetration (IVIS) were evaluated. Molecular analyses including Western blot, qPCR, and immunofluorescence assessed BDNF signaling, tight junction integrity, inflammation, apoptosis, and neurogenesis.
Results: The MagStim+BDNF group exhibited significantly higher BDNF uptake in the ipsi-lesional brain compared to the BDNF-only group. Notably, only MagStim+BDNF treatment markedly reduced infarct volumes and significantly improved motor function and NDS scores; BDNF alone showed no significant difference from Control. The approach was safe, as MagStim did not compromise BBB integrity. Molecularly, MagStim+BDNF preserved tight junction proteins, suppressed inflammatory cytokines and apoptosis, and upregulated neurogenesis and neuronal survival markers in the peri-infarct region.
Conclusion: Focused magnetic stimulation transiently modulates the BBB to amplify BDNF efficacy, providing synergistic neuroprotective and neurorestorative effects. This non-invasive strategy offers a promising translational platform for targeted delivery of neurotrophic factors during subacute stroke recovery.
Methods: Transient middle cerebral artery occlusion (MCAO) was induced in rats. Fourteen days post-stroke, animals were assigned to four groups: Sham, MCAO Control, BDNF alone (intravenous), and MagStim+BDNF (MagStim immediately before intravenous BDNF). Infarct volume (TTC/MRI), neurological function (rotarod/NDS), and BDNF brain penetration (IVIS) were evaluated. Molecular analyses including Western blot, qPCR, and immunofluorescence assessed BDNF signaling, tight junction integrity, inflammation, apoptosis, and neurogenesis.
Results: The MagStim+BDNF group exhibited significantly higher BDNF uptake in the ipsi-lesional brain compared to the BDNF-only group. Notably, only MagStim+BDNF treatment markedly reduced infarct volumes and significantly improved motor function and NDS scores; BDNF alone showed no significant difference from Control. The approach was safe, as MagStim did not compromise BBB integrity. Molecularly, MagStim+BDNF preserved tight junction proteins, suppressed inflammatory cytokines and apoptosis, and upregulated neurogenesis and neuronal survival markers in the peri-infarct region.
Conclusion: Focused magnetic stimulation transiently modulates the BBB to amplify BDNF efficacy, providing synergistic neuroprotective and neurorestorative effects. This non-invasive strategy offers a promising translational platform for targeted delivery of neurotrophic factors during subacute stroke recovery.
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