APPswe/PS1dE9/Blg Transgenic Mouse Line for Modeling Cerebral Amyloid Angiopathy Associated with Alzheimer's Disease

被引:0
|
作者
Lysikova, E. A. [1 ]
Kuzubova, E. V. [2 ]
Radchenko, A. I. [2 ]
Patrakhanov, E. A. [2 ]
Chaprov, K. D. [1 ,2 ]
Korokin, M. V. [2 ]
Deykin, A. V. [2 ]
Gudyrev, O. S. [2 ]
Pokrovskii, M. V. [2 ]
机构
[1] Russian Acad Sci, Inst Physiol Act Cpds, Chernogolovka 142432, Russia
[2] Belgorod State Univ, Belgorod 308015, Russia
关键词
Alzheimer's disease; transgenic mice; amyloid beta; cerebral amyloid angiopathy; PRECURSOR-PROTEIN; BETA-PROTEIN; A-BETA; MICE; AGGREGATION; PRESENILINS; DEPOSITION; PHENOTYPE; PLAQUES;
D O I
10.1134/S0026893323010077
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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 beta (A beta) 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 Ab. Amyloid plaques form in the brains of transgenic mice with overexpression of human Ab, 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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页码:74 / 82
页数:9
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