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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

低氧预处理可改善AβPP/ PS1转基因小鼠的淀粉样β病理和长期认知功能下降。

卷 17, 期 7, 2020

页: [626 - 634] 页: 9

弟呕挨: 10.2174/1567205017666201007121730

价格: $65

摘要

背景与目的：基于中枢神经系统（CNS）缺氧和缺血性疾病的模型，已经建立了低氧预处理（HPC）来触发神经保护的内源性机制。但是，其对阿尔茨海默氏病（AD）的作用仍缺乏实质性证据和深入研究。本研究旨在研究HPC对AβPP/ PS1转基因小鼠AD相关记忆力下降和淀粉样β（Aβ）病理学的影响。 方法：将7周龄的AβPP/ PS1转基因小鼠随机分为HPC组和非HPC组。 HPC组接受早期和重复性HPC治疗4周，而非HPC组则在常氧条件下生长。然后将所有动物饲养到28周龄，之后进行莫里斯水迷宫测试以检查动物的空间记忆。测量了Aβ病理学指标（可溶性Aβ水平和Aβ斑块数量）和相关蛋白的表达，以探索潜在的机制。 结果：结果表明，HPC改善了AβPP/ PS1小鼠的记忆力下降和Aβ病理。在HPC组中，淀粉样β蛋白前体蛋白（AβPP）和β位APP裂解酶1（BACE1）的蛋白水平降低，而低氧诱导因子1α（HIF-1α）的蛋白水平升高。 结论：HPC可能是一种有前途的AD干预策略。它的潜在保护作用可能是通过下调AβPP和BACE1的表达从而抑制Aβ病理学来实现的。值得注意的是，HIF-1α可能在介导HPC继发的神经适应性变化中起关键作用。

关键词: 缺氧预处理，阿尔茨海默氏病，Aβ病理学，缺氧诱导因子1α，痴呆，保护因子。

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