2. Academic Validation
  3. Repetitive Transcranial Magnetic Stimulation Induces Cognitive Recovery in Alzheimer's Disease via GABAergic Neuron Activation of the Cx3cl1-Cx3cr1 Axis

Repetitive Transcranial Magnetic Stimulation Induces Cognitive Recovery in Alzheimer's Disease via GABAergic Neuron Activation of the Cx3cl1-Cx3cr1 Axis

  • Cell Prolif. 2025 May 25:e70061. doi: 10.1111/cpr.70061.
Yunxiao Kang 1 2,  Jilun Liu 3,  Yu Wang 1,  Jiaying Wang 1,  Jinyang Wang 4,  Chenming Zhou 5,  Rui Cui 2 6,  Tianyun Zhang 1 7 8
Affiliations

Affiliations

  • 1 Laboratory of Neurobiology, Hebei Medical University, Shijiazhuang, China.
  • 2 Neuroscience Research Center, Hebei Medical University, Shijiazhuang, China.
  • 3 Department of Oral and Maxillofacial Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
  • 4 Department of Neurology, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
  • 5 Core Facilities and Centers, Hebei Medical University, Shijiazhuang, China.
  • 6 Department of Human Anatomy, Hebei Medical University, Shijiazhuang, China.
  • 7 The Key Laboratory of Neural and Vascular Biology, Ministry of Education, Center for Brain Science and Disease, Hebei Medical University, Shijiazhuang, China.
  • 8 Key Laboratory of Vascular Biology of Hebei Province, Hebei Medical University, Shijiazhuang, China.
PMID: 40415257 DOI: 10.1111/cpr.70061
Abstract

This study aimed to investigate the impact of repetitive transcranial magnetic stimulation (rTMS) on cognitive recovery in Alzheimer's disease (AD) by exploring the role of GABAergic neuron activation and modulation of the Cx3cl1-Cx3cr1 signalling axis. The 5xFAD mouse model was utilised for scRNA-seq analysis to examine changes in gene expression post-rTMS. Microglial phagocytic activity, amyloid plaque burden, cell-cell communication, microglial morphology and neuroinflammation markers were assessed. Following rTMS, upregulation of CX3CL1 in GABAergic neurons was observed, leading to enhanced microglial phagocytosis, reduced amyloid plaque burden, improved cell-cell communication, altered microglial morphology and decreased neuroinflammation markers. This study demonstrates that rTMS promotes Aβ clearance and cognitive recovery in AD by activating GABAergic neurons and enhancing Cx3cl1-Cx3cr1 signalling, providing a novel molecular target for non-invasive AD therapy. These findings support the transition from invasive to non-invasive AD treatments, improving patient adherence and therapeutic outcomes. Furthermore, the elucidation of cellular and molecular mechanisms facilitates drug development targeting the Cx3cl1-Cx3cr1 axis, offering new opportunities for AD intervention.

Keywords

Alzheimer's disease; Cx3cl1‐Cx3cr1 axis; GABAergic neurons; cognitive function; microglia; rTMS.

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