B2肾上腺素能受体基因敲除小鼠早老素1突变体和淀粉样前体蛋白突变体基因差异表达谱

Yuan Zhou, Lintao Chen, Xi Zhou, Yechun Pei, Shuangshuang Wei, Anum Mehmood, Yang K Xiang, Dayong Wang
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引用次数: 1

摘要

阿尔茨海默病(AD)是一种终身进行性神经退行性疾病,与大脑中淀粉样蛋白前体蛋白(APP)加工产生的β淀粉样肽(a β)积累有关。尽管人们对阿尔茨海默病进行了几十年的研究,但仍没有药物用于干预其病理过程。我们在早老素1突变体和淀粉样前体蛋白(APP)家族性AD基因转基因动物模型中进行的研究表明,β2AR基因敲除(β2AR- ko)对老年AD动物有益。一项持续20年的流行病学研究一致表明,单纯使用β受体阻滞剂作为抗高血压药物与老年AD患者的脑损伤和脑萎缩减少有关。为了了解老年β2AR-KO AD小鼠具有更好学习记忆能力的原因,我们研究了β2AR-KO在双转基因AD小鼠中的基因组效应。在分析中,β 2ar - ko的主要基因组意义被指向影响蛋白质加工和递呈,包括膜结构和MHC I类和II类蛋白复合物,以及蛋白质降解的溶酶体和水解酶活性,这对淀粉样β肽的积累至关重要,淀粉样β肽是AD的标志。
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Profiling of Differential Expression of Genes in Mice Carrying Both Mutant Presenilin 1 and Amyloid Precursor Protein Transgenes with or without Knockout of B2 Adrenergic Receptor Gene.

Alzheimer's disease (AD) is a lifelong progressive neurodegenerativa disease related with accumulation of amyloid β peptide (Aβ) produced by processing of amyloid precursor protein (APP) in the brain. In spite of several-decades effort on AD, there is still no medicine used to intervene with its pathological processes. Our previous studies made in transgenic animal models harboring familial AD genes of mutant presenilin 1 and amyloid precursor protein (APP) showed that β2AR gene knock-out (β2AR-KO) is beneficial in senile AD animals. Consistently, an epidemiological study lasted for two decades showed that the sole usage of β blockers as antihypertensive medicines is associated with fewer brain lesions and less brain shrinkage seen in senile AD patients. In order to understand why senile β2AR-KO AD mice had better learning and memory, genomic effects of β2AR-KO in the double transgenic AD mice were investigated. In the analysis, major genomic significance of β2AR-KO was directed to influence protein-processing and presentation involving membrane structure and MHC class I and II protein complex, and lysosome and hydrolase activity for protein degradation, which are critical for accumulation of amyloid β peptide, the hallmark of AD.

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