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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

APP/PS1基因-环境噪声交互作用通过激活VDAC1正反馈环路加重海马ad样神经病理

卷 18, 期 1, 2021

发表于: 24 March, 2021

页: [14 - 24] 页: 11

弟呕挨: 10.2174/1567205018666210324114153

价格: $65

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摘要

背景：环境风险因素，包括环境噪声压力和遗传因素，已经与阿尔茨海默病(AD)的发生和发展有关。然而，环境噪声与APP/PS1基因的环境-基因相互作用导致ad样病理的确切作用和机制尚不清楚。 方法：在此，我们研究了慢性噪声暴露对APP/PS1转基因小鼠ad样神经病理的影响。Morris水迷宫(MWM)任务用于评价ad样变化。对海马磷酸化Tau蛋白、淀粉样蛋白-β (Aβ)和神经炎症进行评估。我们还评估了电压依赖的负离子通道1 (VDAC1)的正反馈环路信号的变化，以探索ad样神经病理与噪声- app /PS1相互作用的潜在机制。 结果：长期噪声暴露显著增加了MWM任务的逃逸延迟和平台跨越次数。在APP/PS1小鼠海马中诱导Aβ过量产生，同时Tau蛋白Ser396和Thr231位点磷酸化增加，小胶质细胞和星形胶质细胞标志物表达增加。此外，噪声暴露后APP/PS1小鼠海马VDAC1-AKT(蛋白激酶B)-GSK3β(糖原合酶激酶3β)-VDAC1信号通路异常激活。 结论：慢性噪声暴露和APP/PS1过表达可协同加重AD患者的认知功能损害和神经病理改变。这种相互作用可能是由VDAC1-AKT-GSK3β-VDAC1信号通路的正反馈环路介导的。

关键词: APP/PS1、慢性噪声、ad样神经病理学、协同效应、基因-环境交互作用、阿尔茨海默病

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