Evidence map›Paper›PMID 41350451›Full record

ArticleMolecular neurobiology2025

iTBS Improves Behavioral Abnormalities and Synaptic Defects in Fmr1 KO Rats by Regulating the Autophagy Pathway.

Zhaonian Deng, Shuaiju Wu, Yaqing Zhao, Anning Song, Hongzheng Wu, Zipei An, Fengru Wang, Xinxin Xu

Abstract read
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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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Zhaonian Deng *State Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China.
Shuaiju Wu *State Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China.
Yaqing ZhaoState Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China.
Anning SongState Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China.
Hongzheng WuState Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China.
Zipei AnState Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China.
Fengru WangState Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China.
Xinxin XuState Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, 300130, China. 2021098@hebut.edu.cn.

Funding

Hebei Natural Science Foundation F2024202082National Natural Science Foundation of China 5240071657the Hebei Central Government Guides Local Science and Technology Development Fund Projects 246Z2511G
6 · The paper itself

Abstract

Synaptic dysfunction resulting from abnormal autophagy may contribute to the pathogenesis of fragile X syndrome (FXS). Intermittent theta burst stimulation (iTBS) is a novel magnetic stimulation mode that has shown promising therapeutic potential in various neurological disorders. However, the therapeutic effects of iTBS on FXS-related behavior abnormality and its underlying mechanism remain unclear. In this study, we investigated whether iTBS could ameliorate behavioral abnormalities and synaptic dysfunction associated with FXS by modulating the autophagy pathway. This study utilized Fmr1 knockout (KO) rats as experimental models. The rats underwent a 2-week iTBS intervention, and behavioral changes were assessed through a series of behavioral tests. Electrophysiological recordings were performed to examine alterations in hippocampal neural oscillations. Golgi staining and Western blotting were utilized to evaluate changes in synaptic structure and synaptic related proteins, while Western blotting and immunofluorescence were employed to assess alterations in autophagy-related proteins. Our results demonstrated that iTBS significantly improved behavioral deficits in Fmr1 KO rats. Furthermore, iTBS effectively attenuated abnormally heightened hippocampal theta-gamma phase-amplitude coupling in these rats. Treatment with iTBS also led to sustained improvements in synaptic defect, along with the restoration of CaMKK2 activity and autophagy defect in the hippocampus of Fmr1 KO rats. These findings underscored the beneficial effects of iTBS on aberrant behavior and synaptic defects in Fmr1 KO rats, highlighting the involvement of the CaMKK2-dependent autophagy pathway in this process and suggesting the potential therapeutic value of iTBS for individuals with FXS.

Indexed as

AutophagyBehavior, AnimalFragile X Messenger Ribonucleoprotein 1SynapsesTranscranial Magnetic StimulationAnimalsFragile X SyndromeGene Knockout TechniquesHippocampusMaleRatsRats, Sprague-DawleyFmr1 protein, ratFragile X Messenger Ribonucleoprotein 1AutophagyFXSITBSNerve oscillationsSocial behaviorSynaptic defects

Identifiers

PMID41350451

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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.