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Changes in Chemokines and Chemokine Receptors Expression in a Mouse Model of Alzheimer's Disease

机译:阿尔茨海默氏病小鼠模型中趋化因子和趋化因子受体表达的变化

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摘要

The amyloid precursor protein plus presenilin-1 (APP/PS1) mice are a frequently-used model for Alzheimer's disease studies (AD). However, the data relevant to which proteins are involved in inflammatory mechanism are not sufficiently well-studied using the AD mouse model. Using behavioral studies, quantitative RT-PCR and Western-blot techniques, significant findings were determined by the expression of proteins involved in inflammation comparing APP/PS1 and Wild type mice. Increased GFAP expression could be associated with the elevation in number of reactive astrocytes. IL-3 is involved in inflammation and ABDF1 intervenes normally in the transport across cell membranes and both were found up-regulated in APP/PS1 mice compared to Wild type mice. Furthermore, CCR5 expression was decreased and both CCL3 and CCL4 chemokines were highly expressed indicating a possible gliosis and probably an increase in chemotaxis from lymphocytes and T cell generation. We also noted for the first time, a CCR8 increase expression with diminution of its CCL1 chemokine, both normally involved in protection from bacterial infection and demyelination. Control of inflammatory proteins will be the next step in understanding the progression of AD and also in determining the mechanisms that can develop in this disease.
机译:淀粉样蛋白前体蛋白加早老素-1(APP / PS1)小鼠是阿尔茨海默氏病研究(AD)的常用模型。但是,使用AD小鼠模型尚未充分研究与哪些蛋白质参与炎症机制有关的数据。通过使用行为研究,定量RT-PCR和Western印迹技术,通过比较APP / PS1和野生型小鼠的炎症相关蛋白的表达确定了重要发现。 GFAP表达增加可能与反应性星形胶质细胞数量的增加有关。 IL-3参与炎症反应,ABDF1通常干预跨细胞膜的转运,与野生型小鼠相比,APP / PS1小鼠中的两种都上调。此外,CCR5表达降低,并且CCL3和CCL4趋化因子均高表达,表明可能是神经胶质增生,并且可能是淋巴细胞和T细胞生成的趋化性增加。我们还首次注意到,CCR8的表达随其CCL1趋化因子的减少而增加,这两者通常都涉及保护免受细菌感染和脱髓鞘作用。炎症蛋白的控制将是理解AD进展以及确定可在这种疾病中发展的机制的下一步。

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