ArticleMolecular brain2025
Effects of intermittent theta burst stimulation on the inflammatory response and cerebral blood flow in promoting neurovascular repair after ischemic stroke.
Article in Molecular brain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Multiscale Mechanisms that Underlie Intermittent Theta-burst Stimulation in Post-stroke Motor Recovery: From Molecular Signaling to Network Reorganization.Translational stroke research · 2026Review
- Intermittent Theta-Burst Stimulation (iTBS) Improves Motor Coordination and Modulates Neuroinflammation and Autophagy in SCA3/MJD Mice.Cerebellum (London, England) · 2026Article
- Non-invasive brain stimulation in frontotemporal dementia: syndrome-specific signals and priorities for future trials.Frontiers in aging neuroscience · 2026Review
- The role of astrocytes in ischemic stroke - mechanisms, functions and treatment.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Secondary injuries from ischemia‒reperfusion in stroke, such as edema and hemorrhagic transformation, can significantly impact brain function. This study investigated the effects of intermittent theta burst stimulation (iTBS) on neurological function and cerebral blood flow in a mouse model of ischemia‒reperfusion injury. Laser speckle flowmetry was used to assess changes in cortical blood flow before and after ischemia‒reperfusion. Behavioral assessments were conducted to evaluate motor function recovery. The impact of iTBS on neuronal damage and apoptosis in the peri-infarct area was evaluated via Nissl staining and a TUNEL assay. RNA transcriptome sequencing and immunofluorescence staining were performed to investigate the effects of iTBS on microglial and astrocyte activation and the associated inflammatory response. Our findings demonstrated that iTBS significantly mitigated abnormal perfusion in the infarcted hemisphere, reduced neuronal damage and apoptosis in the peri-infarct area, and enhanced motor function in ischemic mice. Furthermore, iTBS promoted the polarization of microglia and astrocytes toward the anti-inflammatory M2 and A2 phenotypes. Therefore, iTBS provides neurovascular protection by modulating microglial and astrocyte activation and regulating the inflammatory response in the peri-infarct area, thereby improving abnormal cerebral blood flow in both the acute and subacute phases after ischemic brain injury.
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Registered trials
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