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1950 MHz Electromagnetic Fields Ameliorate Aβ Pathology in Alzheimer’s Disease Mice

机译:1950 MHz电磁场改善了阿尔茨海默氏病小鼠的Aβ病理

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摘要

The involvement of radiofrequency electromagnetic fields (RF-EMF) in the neurodegenerative disease, especially Alzheimer’s disease (AD), has received wide consideration, however, outcomes from several researches have not shown consistency. In this study, we determined whether RF-EMF influenced AD pathology in vivo using Tg-5xFAD mice as a model of AD-like amyloid β (Aβ) pathology. The transgenic (Tg)-5xFAD and wild type (WT) mice were chronically exposed to RF-EMF for 8 months (1950 MHz, SAR 5W/kg, 2 hrs/day, 5 days/week). Notably, chronic RF-EMF exposure significantly reduced not only Aβ plaques, APP, and APP carboxyl-terminal fragments (CTFs) in whole brain including hippocampus and entorhinal cortex but also the ratio of Aβ42 and Aβ40 peptide in the hippocampus of Tg-5xFAD mice. We also found that parenchymal expression of β-amyloid precursor protein cleaving enzyme 1(BACE1) and neuroinflammation were inhibited by RF-EMF exposure in Tg-5xFAD. In addition, RF-EMF was shown to rescue memory impairment in Tg-5xFAD. Moreover, gene profiling from microarray data using hippocampus of WT and Tg-5xFAD following RF-EMF exposure revealed that 5 genes (Tshz2, Gm12695, St3gal1, Isx and Tll1), which are involved in Aβ, are significantly altered inTg-5xFAD mice, exhibiting different responses to RF-EMF in WT or Tg-5xFAD mice; RF-EMF exposure in WT mice showed similar patterns to control Tg-5xFAD mice, however, RF-EMF exposure in Tg-5xFAD mice showed opposite expression patterns. These findings indicate that chronic RF-EMF exposure directly affects Aβ pathology in AD but not in normal brain. Therefore, RF-EMF has preventive effects against AD-like pathology in advanced AD mice with a high expression of Aβ, which suggests that RF-EMF can have a beneficial influence on AD.
机译:射频电磁场(RF-EMF)参与神经退行性疾病,尤其是阿尔茨海默氏病(AD),已得到广泛的考虑,但是,一些研究的结果尚未显示出一致性。在这项研究中,我们确定了RF-EMF是否会使用Tg-5xFAD小鼠作为AD样淀粉样β(Aβ)病理模型来体内影响AD病理。将转基因(Tg)-5xFAD和野生型(WT)小鼠长期暴露于RF-EMF 8个月(1950 MHz,SAR 5W / kg,2小时/天,5天/周)。值得注意的是,长期暴露于RF-EMF不仅显着降低了包括Tg-5xFAD小鼠海马中的Aβ斑块,APP和APP羧基末端片段(CTF),包括海马和内嗅皮层,而且还降低了海马中Aβ42和Aβ40肽的比例。我们还发现,Tg-5xFAD中的RF-EMF暴露抑制了β-淀粉样蛋白前体蛋白裂解酶1(BACE1)的实质表达和神经炎症。此外,RF-EMF被证明可以挽救Tg-5xFAD中的记忆障碍。此外,在RF-EMF暴露后,使用WT和Tg-5xFAD的海马从微阵列数据中进行基因分析,发现与Aβ有关的5个基因(Tshz2,Gm12695,St3gal1,Isx和Tll1)在Tg-5xFAD小鼠中发生了显着改变,在WT或Tg-5xFAD小鼠中表现出对RF-EMF的不同反应; WT小鼠的RF-EMF暴露显示与对照Tg-5xFAD小鼠相似的模式,但是,Tg-5xFAD小鼠的RF-EMF暴露显示相反的表达模式。这些发现表明,长期暴露于RF-EMF会直接影响AD的Aβ病理,但不会影响正常大脑。因此,RF-EMF对具有高表达Aβ的晚期AD小鼠具有预防AD样病理的作用,这表明RF-EMF可以对AD具有有益的影响。

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