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ORIGINAL RESEARCH article

Front. Aging Neurosci.

Sec. Parkinson’s Disease and Aging-related Movement Disorders

Volume 17 - 2025 | doi: 10.3389/fnagi.2025.1524755

This article is part of the Research Topic Transcranial Magnetic Stimulation (TMS) in Motor Control and Motor Rehabilitation: Current Trends and Future Directions View all 8 articles

Role of right dorsolateral prefrontal cortex-left primary motor cortex interaction in motor inhibition in Parkinson's disease

Provisionally accepted
Zhen Wang Zhen Wang 1,2Jianing Wei Jianing Wei 3*Yuyu Song Yuyu Song 2*Yuting Li Yuting Li 2,4Yin Wu Yin Wu 2Robert Chen Robert Chen 5,6Zhen Wang Zhen Wang 2Jian Zhang Jian Zhang 2Xiaoyin Tan Xiaoyin Tan 7*Ke Liu Ke Liu 8*
  • 1 Xi'an Physical Education University, Xi'an, Shaanxi Province, China
  • 2 Shanghai University of Sport, Shanghai, Shanghai Municipality, China
  • 3 Henan University of Science and Technology, Luoyang, Henan Province, China
  • 4 Anhui University of Chinese Medicine, Hefei, Anhui Province, China
  • 5 University Health Network (UHN), Toronto, Ontario, Canada
  • 6 University of Toronto, Toronto, Ontario, Canada
  • 7 Macao Polytechnic University, Macau, Macao, SAR China
  • 8 Shanghai Punan Hospital of Pudong New District, Shanghai, China

The final, formatted version of the article will be published soon.

    Background: Impaired motor inhibition in Parkinson's disease (PD) is associated with functional alterations in the frontal-basal ganglia (BG) neural circuits. The right dorsolateral prefrontal cortex (DLPFC), pre-supplementary motor area (pre-SMA), and primary motor cortex (M1) play key roles in regulating this inhibition. However, the changes in interhemispheric interactions during motor inhibition in PD have not been clearly defined.Methods: We used dual-site paired-pulse transcranial magnetic stimulation (ppTMS) to examine the interactions between the right DLPFC and pre-SMA and the left M1 in 30 patients with early-stage PD and 30 age-matched healthy controls (HC) during both resting and active conditions, specifically while performing a stop-signal task (SST).Results: Stop-signal reaction times (SSRT) were significantly longer in PD patients compared to HC. The right DLPFC–left M1 interaction, at both short- and long-latency intervals, showed enhanced inhibition in PD following the stop-signal. In PD patients, SSRT was correlated with the inhibition of the right DLPFC–left M1 interaction, with stronger inhibition associated with shorter SSRT.Conclusions: The deficit in reactive inhibition observed in PD is linked to an abnormal modulation of the right DLPFC–left M1 interaction during the stopping process.

    Keywords: Parkinson's disease, motor inhibition, Interhemispheric interaction, dorsolateral prefrontal cortex, pre-supplementary motor area

    Received: 19 Nov 2024; Accepted: 18 Feb 2025.

    Copyright: © 2025 Wang, Wei, Song, Li, Wu, Chen, Wang, Zhang, Tan and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Jianing Wei, Henan University of Science and Technology, Luoyang, 471003, Henan Province, China
    Yuyu Song, Shanghai University of Sport, Shanghai, 200072, Shanghai Municipality, China
    Xiaoyin Tan, Macao Polytechnic University, Macau, Macao, SAR China
    Ke Liu, Shanghai Punan Hospital of Pudong New District, Shanghai, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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