Department of Neurology, Affiliated Jinling Hospital, Medical School, Nanjing University, Nanjing, Jiangsu 210000, China.
Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210000, China.
Exp Neurol. 2025 Jan;383:115022. doi: 10.1016/j.expneurol.2024.115022. Epub 2024 Oct 22.
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.
血管性认知障碍和痴呆(VCID)主要由慢性脑灌注不足和随后的白质病变引起。非侵入性经颅磁刺激已被用于治疗各种神经疾病。然而,θ爆发经颅磁刺激对 VCID 的作用仍有待确定。我们利用雄性小鼠双侧颈总动脉狭窄 4 周模型模拟 VCID。给予间歇性 theta 爆发刺激(iTBS)或连续 theta 爆发刺激(cTBS)共 14 天。通过洛索夫快速蓝染色、电子显微镜和免疫荧光,我们发现 iTBS 而非 cTBS 可显著改善脱髓鞘、轴突损伤和 β-淀粉样蛋白沉积,而不影响 VCID 小鼠的脑血流。在细胞水平上,iTBS 挽救了成熟少突胶质细胞的丢失,促进了前体细胞的分化,并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 可减轻 VCID 小鼠短期记忆和长期空间记忆的认知恶化,这通过一系列神经行为测试得到证实。为了探讨 iTBS 的分子机制,我们进行了 mRNA 测序。通过实时 PCR 和结合 RNA 荧光原位杂交与免疫荧光,我们证实 iTBS 特异性地增加了成熟少突胶质细胞中 Rxrg 的表达。综上所述,iTBS 可改善血管性认知功能障碍,可能通过减轻胼胝体的白质病变和神经炎症。iTBS 增加的成熟少突胶质细胞中的 Rxrg 信号可能是 VCID 治疗的潜在靶点。