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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

在阿尔茨海默病体外模型中，磷酸胆碱对淀粉样蛋白 β 神经毒性的有益作用

卷 18, 期 4, 2021

发表于: 23 September, 2021

页: [298 - 309] 页: 12

弟呕挨: 10.2174/1567205018666210608093658

价格: $65

摘要

背景：阿尔茨海默病 (AD) 是最常见的以认知障碍为特征的神经退行性疾病，这是一个紧迫的公共卫生问题。鉴于 AD 的全球影响，迫切需要有效的疗法来减缓或阻止这种疾病。

目的：磷酸胆碱 (α-GPC) 是一种潜在有效的胆碱能神经传递增强剂，在改善认知功能障碍方面具有有趣的临床特征，尽管关于这种有益作用背后的机制的数据很少。

方法：将 SH-SY5Y 神经元细胞系用 10 μm 全反式维甲酸 (RA) 分化 1 周，以实现向胆碱能表型的转变，用作 AD 的体外模型。 SH-SY5Y细胞用α-GPC（100nM）预处理1小时，用Aβ25-35（10μM）处理72小时。

结果：α-GPC 能够拮抗 Aβ25-35 介导的神经毒性并减弱 Aβ 诱导的 Tau 蛋白磷酸化。此外，α-GPC 通过使用 NGF/TrkA 系统发挥其有益作用，在 AD 中被击倒，因此，通过维持突触囊泡蛋白（如突触素）的表达水平。

结论：综上所述，我们的数据表明，α-GPC 在 Aβ 毒性挑战过程中可以起到神经保护作用。因此，更深入地了解其有益作用的机制，可以为其功能性胆碱能增强的潜在未来药理学应用提供新的见解，旨在减轻 AD，并可能代表创新疗法的基础。

关键词: 乙酰胆碱、细胞凋亡、胆碱能神经传递、神经元、突触发生、阿尔茨海默病。

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