摘要
背景:与瑞典突变(Appswe)和外显子9缺失早产儿(Ps1dE9)共同表达人淀粉样前体蛋白的小鼠已成为目前应用最广泛的小鼠模型之一。 g阿尔茨海默病(AD)发病机制及AD治疗途径的临床前研究。 目的:系统研究APPswe/PS1dE9中的认知功能减退、淀粉样蛋白(Aβ-β,Aβ)沉积与脑或A型β水平的关系及其相互关系。 转基因小鼠。 方法:将APPswe/PS1dE9小鼠分为4、6、9、12个月龄组。我们评估了脑组织和血清中的认知能力、沉积的斑块以及Aβ40/Aβ42的水平。 不同年龄的老鼠。 结果:APPswe/PS1dE9小鼠从6月龄开始记忆能力下降,12个月时认知能力明显受损。巧合的是,淀粉样沉积开始在运输过程中发育。 6月龄NIC小鼠脑组织随年龄增加而增加。此外,APPswe/PS1dE9小鼠脑内Aβ42水平随年龄增加而升高,而Aβ40则无相应增加。血清Aβ42 DELI浓度 Ned在4~6个月大,但Aβ40无类似的年龄依赖性下降。 结论:APPswe/PS1dE9转基因小鼠在6月龄开始发育淀粉样斑块,并表现出相应的空间学习能力障碍。血清Aβ42水平显著下降 Ly期为4~6个月,A期β42开始在脑内积聚,并以斑块的形式沉积。
关键词: 阿尔茨海默病,淀粉样沉积,APPswe/PS1dE9转基因小鼠,脑Aβ42,认知功能减退,血清Aβ42。
Current Alzheimer Research
Title:Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice
Volume: 15 Issue: 11
关键词: 阿尔茨海默病,淀粉样沉积,APPswe/PS1dE9转基因小鼠,脑Aβ42,认知功能减退,血清Aβ42。
摘要: Background: Mice co-expressing human amyloid precursor protein with the Swedish mutation (APPswe) and exon-9-deleted presenilin (PS1dE9) has become one of the most widely used mouse models for studying Alzheimer’s disease (AD) pathogenesis and preclinical studies of AD therapeutic approaches.
Objective: In this study, we systematically investigated cognitive decline, amyloid-β (Aβ) deposition and cerebral or Aβ serum levels as well as the relationships among these measures in APPswe/PS1dE9 transgenic mice.
Method: APPswe/PS1dE9 mice were separated into four equal age cohorts (4, 6, 9, and 12 months). We assessed cognitive capacity, deposited plaques, and the levels of Aβ40/Aβ42 in brain tissue and serum of mice at different ages.
Results: APPswe/PS1dE9 mice exhibited declined memory beginning at 6 months of age, with cognitive capacity remarkably impaired at 12-months. Coincidently, amyloid deposits began to develop in transgenic mice brain at 6-months and increased with age. In addition, Aβ42 levels in brains of APPswe/ PS1dE9 mice increased with age with no parallel increase in Aβ40. The concentration of serum Aβ42 declined from 4 to 6 months of age, but a similar age-dependent decrease was not observed for Aβ40.
Conclusion: APPswe/PS1dE9 transgenic mice began to develop amyloid plaques at 6 months of age and exhibited a corresponding impairment of spatial learning capacity. Serum Aβ42 level decreased remarkably from 4 to 6 months, at which stage Aβ42 began to accumulate in the brain and deposit as plaques.
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Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice, Current Alzheimer Research 2018; 15 (11) . https://dx.doi.org/10.2174/1567205015666180709112327
DOI https://dx.doi.org/10.2174/1567205015666180709112327 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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