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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

脊髓损伤对阿尔茨海默氏病TgCRND8小鼠模型中β-淀粉样蛋白斑块病理的影响

卷 17, 期 6, 2020

页: [576 - 586] 页: 11

弟呕挨: 10.2174/1567205017666200807191447

价格: $65

摘要

背景：在其他神经系统疾病（例如脑外伤）中，发现了Aβ作为淀粉样斑块的积累和聚集，这是阿尔茨海默氏病的标志性病理。轴突损伤可能有助于Aβ斑块的形成。迄今为止的研究都集中在大脑上，没有对脊髓进行任何研究，尽管大脑和脊髓共享相同的细胞成分。 目的：我们利用脊髓横断模型研究了在TgCRND8转基因AD模型中，脊髓损伤在损伤后3天是否急性诱导Aβ斑块的发作或促进了Aβ斑块的进展。 方法：分别在3和20个月大的TgCRND8小鼠及其同窝出生的野生型小鼠中进行脊髓横切。免疫组织化学反应/ ELISA法测定TgCRND8小鼠脊髓中轴突损伤的程度和Aβ斑块的发生/改变或不同年龄的Aβ水平。 结果：损伤后，在3和20个月大的TgCRND8小鼠的脊髓周围病变区域中观察到APP及其产物Aβ的轴突内共蓄积表明了广泛的轴突病理。匹配的非TgCRND8小鼠。然而，在3个月大的TgCRND8小鼠中未发现Aβ斑块。与邻近于脊髓横断后的假手术小鼠的受伤区域和相应区域的组织相比，在脊髓中已建立淀粉样变性的20个月大的TgCRND8小鼠在病变部位的斑块负担减少而不是增加。与假手术动物相比，受伤小鼠的脊髓区域病变部位被CD68阳性巨噬细胞/活化的小胶质细胞占据。这些结果表明，脊髓损伤不诱导TgCRND8小鼠的脊髓中Aβ斑块的急性发作和进展。相反，它会诱导TgCRND8小鼠Aβ斑块沉积的消退。 结论：这些发现强调了轴突损伤在控制急性Aβ斑块形成中的依赖性，并提供证据表明Aβ斑块病理可能在脊髓损伤后的继发性损伤级联中不起作用。

关键词: 轴突损伤，β淀粉样蛋白，淀粉样前体蛋白，阿尔茨海默氏病，淀粉样蛋白斑块，脊髓损伤。

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