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Memory Impairment in AB (25-35) and D-Galactose Induced Alzheimer's Disease Model Rat

机译:AB(25-35)和D-半乳糖诱导阿尔茨海默病模型大鼠的记忆障碍

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Beta amyloid (Aβ) is a key pathological hallmark of Alzheimer disease (AD) and plays key roles the progressive process of this disease. However the involved biological processes or pathways that triggered by Aβ in the progress of AD are still unclear. To answer this question, Aβ_(25-35) was bilaterally injected into the rats' bilateral hippocampus and to accelerate the brain aging, d-gal was subcutaneously administrated, so as to set up the combined AD model rats and further explore the gene expression profile of the rats. The results demonstrated that the d-gal and Aβ treatment led to learning and memory impairment in behavioral test and neuronal cells damage in the brain, which validated the establishment of AD model rats. These verified genes may provide a new insight for elucidating Aβ cascade hypothesis in AD and its progression.
机译:β淀粉样蛋白(Aβ)是阿尔茨海默病(AD)的关键病理标志,并发挥这种疾病的渐进过程。然而,Aβ在广告进度中触发的涉及的生物过程或途径仍然不清楚。为了回答这个问题,将Aβ(25-35)双侧注射到大鼠的双侧海马中并加速脑老化,D-GAL被皮下给药,以便建立组合的广告模型大鼠并进一步探索基因表达老鼠的概况。结果表明,D-GAL和Aβ治疗导致了在脑部中的行为试验和神经元细胞损伤中的学习和记忆障碍,验证了广告模型大鼠的建立。这些已验证的基因可以提供一种新的洞察,用于阐明AD和其进展中的Aβ级联假设。

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