转基因小鼠
神经退行性变
转基因
淀粉样蛋白(真菌学)
阿尔茨海默病
淀粉样前体蛋白
神经科学
神经炎症
医学
病理
生物
疾病
生物化学
基因
作者
Ekaterina A. Lysikova,Elena Kuzubova,Alexandra Radchenko,E. A Patrakhanov,Kirill D. Chaprov,М. В. Корокин,Alexey V. Deykin,О. С. Гудырев,М. В. Покровский
出处
期刊:PubMed
日期:2023-03-29
卷期号:57 (1): 85-94
被引量:1
标识
DOI:10.31857/s0026898423010081
摘要
Alzheimer's disease (AD) is the most common proteinopathy, which is accompanied by a steady decrease in the patient's cognitive functions with a simultaneous accumulation of amyloid plaques in brain tissues. Amyloid plaques are extracellular aggregates of amyloid β (Aβ) and are associated with neuroinflammation and neurodegeneration. Unlike humans and all other mammals, rats and mice do not reproduce AD-like pathology because there are three amino acid substitutions in their Aβ. Amyloid plaques form in the brains of transgenic mice with overexpression of human Aβ, and such mice are therefore possible to use in biomedicine to model the key features of AD. The transgenic mouse line APPswe/PS1dE9 is widely used as an animal model to study the molecular mechanisms of AD. A study was made to characterize the APPswe/PS1dE9/Blg subline, which was obtained by crossing APPswe/PS1dE9 mice on a CH3 genetic background with C57Bl6/Chg mice. No difference in offspring's survival and fertility was observed in the subline compared to wild-type control mice. Histological analysis of the brain in the APPswe/PS1dE9/Blg line confirmed the main neuromorphological features of AD and showed that amyloid plaques progressively increase in number and size during aging. The APPswe/PS1dE9/Blg line was assumed to provide a convenient model for developing therapeutic strategies to slow down AD progression.
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