ArticleInternational journal of clinical and health psychology : IJCHP
Dual-site beta tACS over rIFG and M1 enhances response inhibition: A parallel multiple control and replication study.
Article in International journal of clinical and health psychology : IJCHP. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Repeated application of bifocal transcranial alternating current stimulation improves network connectivity but not response inhibition: a double-blind sham control study.Cerebral cortex (New York, N.Y. : 1991) · 2025Trial
- Precision non-invasive transcranial electromagnetic stimulation: a thematic review of optimizing spatial, temporal, and dose dimensions.European archives of psychiatry and clinical neuroscience · 2026Review
- Phase-Specific Dual-Site Beta Transcranial Alternating Current Stimulation Differentially Influences Functional Connectivity Associated With Motor Inhibition Performance.Human brain mapping · 2026Article
- Variable E-field properties of dual-site tACS with phase lags.Imaging neuroscience (Cambridge, Mass.) · 2026Article
- Bifocal tACS over the primary sensorimotor cortices increases interhemispheric inhibition and improves bimanual dexterity.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Multifocal transcranial electrical stimulation to enhance cognitive functions: a systematic review.Frontiers in neuroscience · 2025Review
- Comparative efficacy of tDCS and tACS in the context of enhancing executive function under acute stress: A randomized, sham-controlled study.International journal of clinical and health psychology : IJCHPArticle
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7 authors.
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Abstract
Response inhibition is a core component of cognitive control. Past electrophysiology and neuroimaging studies have identified beta oscillations and inhibitory control cortical regions correlated with response inhibition, including the right inferior frontal gyrus (rIFG) and primary motor cortex (M1). Hence, increasing beta activity in multiple brain regions is a potential way to enhance response inhibition. Here, a novel dual-site transcranial alternating current stimulation (tACS) method was used to modulate beta activity over the rIFG-M1 network in a sample of 115 (excluding 2 participants) with multiple control groups and a replicated experimental design. In Experiment 1, 70 healthy participants were randomly assigned to three dual-site beta-tACS groups, including in-phase, anti-phase or sham stimulation. During and after stimulation, participants were required to complete the stop-signal task, and electroencephalography (EEG) was collected before and after stimulation. The Barratt Impulsiveness Scale was completed before the experiment to evaluate participants' impulsiveness. In addition, we conducted an active control experiment with a sample size of 20 to exclude the potential effects of the dual-site tACS "return" electrode. To validate the behavioural findings of Experiment 1, 25 healthy participants took part in Experiment 2 and were randomized into two groups, including in-phase and sham stimulation groups. We found that compared to the sham group, in-phase but not anti-phase beta-tACS significantly improved both response inhibition performance and beta synchronization of the inhibitory control network in Experiment 1. Furthermore, the increased beta synchronization was correlated with enhanced response inhibition. In an independent sample of Experiment 2, the enhanced response inhibition performance observed in the in-phase group was replicated. After combining the data from the above two experiments, the time dynamics analysis revealed that the in-phase beta-tACS effect occurred in the post-stimulation period but not the stimulation period. The state-dependence analysis showed that individuals with poorer baseline response inhibition or higher attentional impulsiveness had greater improvement in response inhibition for the in-phase group. These findings strongly support that response inhibition in healthy adults can be improved by in-phase dual-site beta-tACS of the rIFG-M1 network, and provide a new potential treatment targets of synchronized cortical network activity for patients with clinically deficient response inhibition.
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