θ-脉冲经颅磁刺激可减轻小鼠慢性缺血性脱髓鞘和血管性认知障碍。

IF 4.6 2区 医学 Q1 NEUROSCIENCES
Di Wang , Xiaohao Zhang , Zhenqian Huang , Yunzi Li , Xinyi Wang , Jia Wang , Ying Zhao , Qiushi Lv , Min Wu , Mingming Zha , Kang Yuan , Wusheng Zhu , Gelin Xu , Yi Xie
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引用次数: 0

摘要

血管性认知障碍和痴呆症(VCID)主要是由慢性脑灌注不足和随后的白质病变引起的。无创经颅磁刺激已被用于治疗各种神经系统疾病。然而,θ-脉冲经颅磁刺激对 VCID 的作用仍有待明确。我们利用为期 4 周的雄性小鼠双侧颈动脉狭窄模型模拟 VCID。连续14天给予间歇θ-脉冲刺激(iTBS)或连续θ-脉冲刺激(cTBS)。通过鲁索快蓝染色、电子显微镜和免疫荧光,我们发现iTBS而非cTBS能显著改善VCID小鼠的脱髓鞘、轴突损伤和β淀粉样蛋白沉积,而不影响脑血流量。在细胞水平上,iTBS 挽救了成熟少突胶质细胞的丧失,促进了前体细胞分化,抑制了星形胶质细胞和小胶质细胞的促炎激活。值得注意的是,iTBS 可以减轻 VCID 小鼠短期记忆和长期空间记忆的认知退化,这一点可以通过连续的神经行为测试得到证明。为了探索 iTBS 的分子参与,研究人员进行了 mRNA 测序。通过实时 PCR 和 RNA 荧光原位杂交与免疫荧光相结合的方法,证实 iTBS 能增加 Rxrg 在成熟少突胶质细胞中的特异性表达。总之,iTBS 可以改善血管性认知功能障碍,可能是通过减轻胼胝体的白质病变和神经炎症。iTBS可增加成熟少突胶质细胞中的Rxrg信号转导,这可能是治疗血管性认知功能障碍的潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Theta-burst transcranial magnetic stimulation attenuates chronic ischemic demyelination and vascular cognitive impairment in mice
Vascular cognitive impairment and dementia (VCID) is mainly caused by chronic cerebral hypoperfusion and subsequent white matter lesions. Noninvasive transcranial magnetic stimulation has been utilized in treating various neurological disorders. However, the function of theta-burst transcranial magnetic stimulation on VCID remains to be defined. We utilized 4-week bilateral carotid artery stenosis model of male mice to mimic VCID. Intermittent theta-burst stimulation (iTBS) or consecutive theta-burst stimulation (cTBS) was administered for 14 consecutive days. Through luxol fast blue staining, electron microscopy and immunofluorescence, we found that iTBS, not cTBS, significantly improved demyelination, axonal damage and β-amyloid deposition, without affecting cerebral blood flow in VCID mice. At cellular levels, iTBS rescued the loss of mature oligodendrocytes, promoted precursor cell differentiation, and inhibited pro-inflammatory activation of astrocytes and microglia. Notably, iTBS attenuated cognitive deterioration in both short-term retention and long-term spatial memory of VCID mice as indicated by serial neurobehavioral tests. To explore the molecular involvement of iTBS, mRNA sequencing was carried out. By real-time PCR and combined RNA fluorescence in situ hybridization with immunofluorescence, iTBS was confirmed to increase Rxrg expression specifically in mature oligodendrocytes. Collectively, iTBS could ameliorate vascular cognitive dysfunction, probably via mitigating white matter lesions and neuroinflammation in the corpus callosum. Rxrg signaling in mature oligodendrocytes, which was increased by iTBS, might be a potential target for VCID treatment.
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来源期刊
Experimental Neurology
Experimental Neurology 医学-神经科学
CiteScore
10.10
自引率
3.80%
发文量
258
审稿时长
42 days
期刊介绍: Experimental Neurology, a Journal of Neuroscience Research, publishes original research in neuroscience with a particular emphasis on novel findings in neural development, regeneration, plasticity and transplantation. The journal has focused on research concerning basic mechanisms underlying neurological disorders.
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