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The Neuroprotection of Repetitive Transcranial Magnetic Stimulation Pre-treatment in Vascular Dementia Rats
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  • 作者:Fei Wang (1)
    Guang-ming Chang (2)
    Qian Yu (3)
    Xin Geng (4) (5)

    1. Department of Neurology
    ; General Hospital ; Tianjin Medical University ; Tianjin ; People鈥檚 Republic of China
    2. Department of Clinical Laboratory
    ; General Hospital ; Tianjin Medical University ; Tianjin ; People鈥檚 Republic of China
    3. General Hospital
    ; Tianjin Medical University ; Tianjin ; People鈥檚 Republic of China
    4. Department of Biochemistry and Molecular Biology
    ; Tianjin Medical University ; Tianjin ; People鈥檚 Republic of China
    5. Tianjin Key Laboratory of Cellular and Molecular Immunology
    ; Tianjin ; People鈥檚 Republic of China
  • 关键词:Vascular dementia ; Repetitive transcranial magnetic stimulation ; Brain ; derived neurotrophic factor ; Tyrosine kinase receptor B ; Synaptophysin
  • 刊名:Journal of Molecular Neuroscience
  • 出版年:2015
  • 出版时间:May 2015
  • 年:2015
  • 卷:56
  • 期:1
  • 页码:198-204
  • 全文大小:3,890 KB
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  • 刊物主题:Neurosciences; Neurochemistry; Cell Biology; Proteomics; Neurology;
  • 出版者:Springer US
  • ISSN:1559-1166
文摘
Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive technique that could interfere cortical excitability though brief electric currents induced by alternating magnetic fields from the inductive coil. Currently, it has been applied in many fields of basic and clinical neuro-research. The aims of the present study are to investigate the effect of rTMS pre-treatment on cognitive function in vascular dementia (VaD) rats and further explore the molecular mechanism of rTMS neuroprotection on VaD. We found that rTMS pre-treated VaD rats showed significantly better memory and learning abilities in Morris water maze test compared to the untreated group. Moreover, the mRNA and protein expression levels of BDNF, TrkB, and SYN were significantly higher in the rTMS pre-treated group, indicating that rTMS pre-treatment has neuroprotective effect for VaD, which may have resulted from the increased level of BDNF, TrkB, and SYN in the hippocampal CA1 area.

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