Dysregulation of inflammatory markers like cytokines is implicated in the pathophysiology of Alzheimer's disease (AD). Altered level of these cytokines show that pathogenesis of AD is beyond dysfunction of neurons resulting from amyloid beta accumulation but involves neuroinflammatory mechanisms elicited by the neuroimmune cell. In this study, we investigated the effect of amyloid-beta (1-42) (Aβ(1-42)) on memory and how inflammatory markers respond to this model of AD. Male Sprague-Dawley rats were used for this study. The animals were randomly divided into four groups euthanized on day 3, 7, 10 and 14 post-lesion with amyloid-beta (5 μg/5 μl) while corresponding control groups were stereotaxically injected with a vehicle (5 μl of 0.01 M phosphate- buffered saline). The Morris water maze (MWM) test to access learning and memory was conducted pre and post-lesion and blood was collected through cardiac puncture on day 3, 7, 10 and 14 post lesion. Multiplex immunoassay was performed to determine the plasma levels of IL-1β, IL-6, IL-10 and TNF-α. Our results showed impaired spatial memory and elevated plasma levels of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) with a concomitantly lowered level of the anti-inflammatory cytokine (IL-10) in the Aβ(1-42) lesioned rats when compared to the vehicle groups. This study showed a negative correlation between the decline in performance of the spatial memory task and plasma levels of the pro-inflammatory cytokines IL-1β, IL-6 and TNF-α and positive correlation with the anti-inflammatory cytokine IL-10. In conclusion, this study most importantly demonstrated an association between progressive decline in spatial memory and increased plasma cytokine level induced by the infusion of Aβ(1-42).

中文翻译：

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记忆力下降与阿尔茨海默氏病的淀粉样β（1-42）大鼠模型中血浆细胞因子增加有关。

诸如细胞因子之类的炎症标志物的失调与阿尔茨海默氏病（AD）的病理生理有关。这些细胞因子水平的变化表明，AD的发病机理超出了由淀粉样蛋白β积累引起的神经元功能障碍，但涉及神经免疫细胞引起的神经炎症机制。在这项研究中，我们调查了淀粉样蛋白（1-42）（Aβ（1-42））对记忆的影响以及炎症标记物如何对AD模型做出反应。将雄性Sprague-Dawley大鼠用于该研究。在病变后第3、7、10和14天，将动物随机分为4组，分别用β-淀粉样蛋白（5μg/ 5μl）安乐死，而相应的对照组则通过立体定位注射媒介物（5μl0.01 M磷酸盐-缓冲盐水）。在损伤前和损伤后进行莫里斯水迷宫（MWM）测试，以获取学习和记忆，并在损伤后第3、7、10和14天通过心脏穿刺收集血液。进行多重免疫测定以确定IL-1β，IL-6，IL-10和TNF-α的血浆水平。我们的结果表明，空间记忆受损，促炎细胞因子（IL-1β，IL-6和TNF-α）的血浆水平升高，同时Aβ中抗炎细胞因子（IL-10）的水平降低（1- 42）与媒介物组相比患病的大鼠。这项研究表明，空间记忆任务的下降与促炎细胞因子IL-1β，IL-6和TNF-α的血浆水平之间呈负相关，而与消炎细胞因子IL-10呈正相关。结论，