Transcranial magneto-acoustic stimulation improves corticostriatal transmission in direct medium spiny neurons and rescues neuroplasticity of Parkinson's disease model mice.

Yihao Xu, Shuai Zhang, Jinrui Mi, Xiaochao Lu, Yuchen An, Jizhou Liu, Jiaqi Sun, Yanbin Wang, Guizhi Xu

Abstract read

In one paragraph

Article in NPJ Parkinson's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

9 authors.

Yihao XuSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Shuai ZhangSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China. zs@hebut.edu.cn.

Jinrui MiSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Xiaochao LuSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Yuchen AnSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Jizhou LiuSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Jiaqi SunSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Yanbin WangSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Guizhi XuSchool of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin, China.

Funding

Central Guidance for Local Scientific and Technological Development Foundation of Hebei, China 236Z7711GNational Natural Science Foundation of China 52377224

6 · The paper itself

Abstract

Transcranial magneto-acoustic stimulation (TMAS) is a noninvasive neuromodulation technique that has demonstrated benefits for neuroplasticity in Parkinson's disease (PD), yet its underlying mechanisms remain inadequately understood. This study aimed to investigate how TMAS affects dysfunction and synaptic-plasticity impairments in the corticostriatal pathway in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. The results indicated that TMAS was associated with reduced presynaptic glutamate release and with improved N-methyl-D-aspartate receptor (NMDAR)-mediated responses. It also enhanced D1 dopamine receptor-dependent basal synaptic transmission and partially restored bidirectional corticostriatal synaptic plasticity. Furthermore, TMAS tended to normalize the distribution of spine subtypes, improve motor deficits, reduce dopaminergic neuron loss, and decrease aberrant α-synuclein expression. Transcriptomic and enrichment analyses further suggested a coordinated modulation of gene programs related to synaptic organization, ion homeostasis, and immune responses. These findings support TMAS as a promising noninvasive neuromodulation approach in the MPTP mouse model. TMAS attenuated excessive glutamatergic transmission and improved corticostriatal synaptic plasticity, providing a testable mechanistic framework for future studies.

Identifiers

PMID41922369

DOI10.1038/s41531-026-01333-8

PMCPMC13216318

What Socratic holds

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LicenceCC BY-NC-ND

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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 Socratic graph.