Alzheimer's disease (AD) is a neurodegenerative disorder, characterized by cognitive impairment, progressive neurodegeneration, and amyloid-β (Aβ) lesion. In the neuronal death and disease progression, inflammation is known to play an important role. Our previous study on acute-phase protein serum amyloid A1 (SAA1) overexpressed mice showed that the liver-derived SAA1 accumulated in the brain by crossing the brain blood barrier (BBB) and trigger the depressive-like behavior on mouse. Since SAA1 involved in immune responses in other diseases, we focused on the possibility that SAA1 may exacerbate the neuronal inflammation related to Alzheimer's disease. A APP/SAA overexpressed double transgenic mouse was generated using amyloid precursor protein overexpressed (APP)-c105 mice and SAA1 overexpressed mice to examine the function of SAA1 in Aβ abundant condition. Comparisons between APP and APP/SAA1 transgenic mice showed that SAA1 exacerbated amyloid aggregation and glial activation; which lead to the memory decline. Behavior tests also supported this result. Overall, overexpression of SAA1 intensified the neuronal inflammation in amyloid abundant condition and causes the greater memory decline compared to APP mice, which only expresses Aβ 1-42.

中文翻译：

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血清淀粉样蛋白A1参与淀粉样蛋白丰富条件下的淀粉样蛋白斑块聚集和记忆力下降。

阿尔茨海默氏病（AD）是一种神经退行性疾病，其特征在于认知障碍，进行性神经退行性病变和β-淀粉样蛋白（Aβ）病变。在神经元死亡和疾病进展中，炎症起着重要作用。我们先前对急性期蛋白血清淀粉样蛋白A1（SAA1）过表达的小鼠的研究表明，肝源性SAA1通过穿越脑血屏障（BBB）积聚在大脑中并触发了小鼠的抑郁样行为。由于SAA1参与了其他疾病的免疫反应，因此我们关注SAA1可能加剧与阿尔茨海默氏病相关的神经元炎症的可能性。使用淀粉样前体蛋白过表达（APP）-c105小鼠和SAA1过表达的小鼠生成APP / SAA过表达的双转基因小鼠，以检查SAA1在Aβ丰富条件下的功能。APP和APP / SAA1转基因小鼠的比较表明，SAA1加剧了淀粉样蛋白的聚集和神经胶质的激活。这导致内存下降。行为测试也支持此结果。总体而言，与仅表达Aβ1-42的APP小鼠相比，淀粉样蛋白丰富状态下SAA1的过度表达加剧了神经元炎症，并导致更大的记忆力下降。