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当代阿耳茨海默病研究

Editor-in-Chief

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

General Research Article

淀粉样β诱导的神经毒性损害阿尔茨海默氏病小鼠模型的认知和成人海马神经发生

卷 17, 期 11, 2020

页: [1033 - 1042] 页: 10

弟呕挨: 10.2174/1567205017666201224162730

价格: $65

摘要

背景:神经发生是从现有干细胞壁中产生新神经元的关键机制,在整个成年哺乳动物脑中一直持续存在,尽管会随着衰老或诸如阿尔茨海默氏病(AD)等神经退行性疾病的发展而减速。在过去的几年中,成年海马神经元的受损与淀粉样蛋白β(Aβ)和tau蛋白过度磷酸化引起的神经毒性一起,成为AD病理生理的重要标志。但是,尚无确凿的证据表明在AD进展过程中成年海马神经发生上调/下调。 方法:在这项研究中,我们使用Aβ(1-42)诱导的AD小鼠模型检查了成年海马神经发生和认知功能障碍的变化。 结果:我们的结果表明,在BALB / c小鼠中,Aβ给药可诱发类似行为的焦虑,并损害空间和非空间记忆与学习。在用Aβ处理的动物中,海马的齿状回(DG),CA1,CA2和CA3区也出现了广泛的神经元丢失。此外,Aβ暴露显着降低了细胞增殖和迁移标志物即Ki67和DCX的实时表达,而免疫组织化学分析表明Ki67和NeuN的表达水平显着降低。 结论:我们的发现突出了Aβ诱导的神经毒性与神经发生和记忆形成改变的关系。但是,有必要进一步了解以探索潜在的分子途径。此外,旨在修复成人海马神经发生的治疗策略具有作为AD疗法的潜力。

关键词: 海马,神经退行性变,神经发生,阿尔茨海默氏病,认知,神经毒性。

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