Evidence map›Paper›PMID 39052185›Full record

ArticleMolecular neurobiology2025

Repetitive Transcranial Magnetic Stimulation-Mediated Neuroprotection in the 5xFAD Mouse Model of Alzheimer's Disease Through GABRG2 and SNAP25 Modulation.

Jinyang Wang, Chenming Zhou, Zhimin Huang, Xiaoming Ji, Rui Cui, Yunxiao Kang, Guoliang Zhang, Yu Wang, Tianyun Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Jinyang WangDepartment of Neurology, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
Chenming ZhouCore Facilities and Centers, Hebei Medical University, Shijiazhuang, 050017, China.
Zhimin HuangDepartment of Stomatology, People's Hospital, Shizhu Tujia Autonomous County, Chongqing, 409100, China.
Xiaoming JiLaboratory of Neurobiology, Hebei Medical University, Zhongshan Donglu No.361, ShijiazhuangHebei Province, 050017, China.
Rui CuiNeuroscience Research Center, Hebei Medical University, Shijiazhuang, 050017, China.
Yunxiao KangLaboratory of Neurobiology, Hebei Medical University, Zhongshan Donglu No.361, ShijiazhuangHebei Province, 050017, China.
Guoliang ZhangNeuroscience Research Center, Hebei Medical University, Shijiazhuang, 050017, China.
Yu WangLaboratory of Neurobiology, Hebei Medical University, Zhongshan Donglu No.361, ShijiazhuangHebei Province, 050017, China.
Tianyun ZhangLaboratory of Neurobiology, Hebei Medical University, Zhongshan Donglu No.361, ShijiazhuangHebei Province, 050017, China. zhangtianyun@hebmu.edu.cn.

Funding

Hebei Medical Science Research Project Plan 20240255Hebei Provincial Natural Science Foundation Precision Medicine Joint Fund Cultivation Project H2021206269, H2022206023Scientific Research Projects of Higher Education Institutions in Hebei Province QN2024035
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a leading neurodegenerative disorder with substantial impacts on cognition and behavior. Repetitive transcranial magnetic stimulation (rTMS), a non-invasive neuromodulation technique, has been used to treat various neuropsychiatric disorders, but its efficacy in AD has not been thoroughly investigated. This study examines the neuroprotective effects of rTMS in the 5xFAD mouse model of AD, with a particular focus on its modulation of GABAergic neuronal activity via the GABRG2 and SNAP25 proteins. Transcriptomic sequencing of rTMS-treated 5xFAD mice revealed 32 genes influenced by the treatment, among which GABRG2 was identified as a critical modulatory target. Electrophysiological assessments, including whole-cell patch clamp recordings from frontal cortex neurons, demonstrated significant alterations in inhibitory synaptic currents following rTMS. Subsequent experiments involved sh-GABRG2 transduction combined with rTMS treatment (20Hz, 14 days), examining behavioral responses, GABAergic neuron functionality, cortical GABA expression, cerebrospinal fluid GABA concentrations, β-amyloid accumulation, and pro-inflammatory cytokine levels. The results indicated notable improvements in behavioral performance, enhanced functionality of GABAergic neurons, and reductions in β-amyloid deposition and neuroinflammation after rTMS treatment. Further analysis revealed that SNAP25 overexpression could counteract the negative effects of GABRG2 silencing, highlighting the crucial role of SNAP25 downstream of GABRG2 in mediating rTMS's therapeutic effects in AD. This research highlights rTMS's potential to modulate synaptic and vesicular transport mechanisms, offering a promising avenue for ameliorating symptoms of AD through neuroprotective pathways.

Indexed as

Alzheimer DiseaseNeuroprotectionReceptors, GABA-ASynaptosomal-Associated Protein 25Transcranial Magnetic StimulationAmyloid beta-PeptidesAnimalsDisease Models, AnimalGABAergic Neuronsgamma-Aminobutyric AcidMiceMice, TransgenicAmyloid beta-Peptidesgamma-Aminobutyric AcidReceptors, GABA-ASnap25 protein, mouseSynaptosomal-Associated Protein 25Alzheimer’s diseaseCerebral cortexGABAGABRG2Repetitive transcranial magnetic stimulationSNAP25Synaptic functionVesicular transport

Identifiers

PMID39052185

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.