APPswe/PS1dE9/Blg Transgenic Mouse Line for Modeling Cerebral Amyloid Angiopathy in Alzheimer’s Disease
-
Published:2023-01-01
Issue:1
Volume:57
Page:85-94
-
ISSN:0026-8984
-
Container-title:Молекулярная биология
-
language:
-
Short-container-title:Molekulârnaâ biologiâ
Author:
Lysikova E. A.1, Kuzubova E. V.2, Radchenko A. I.2, Patrakhanov E. A.2, Chaprov K. D.12, Korokin M. V.2, Deykin A. V.2, Gudyrev O. S.2, Pokrovskii M. V.2
Affiliation:
1. Institute of Physiologically Active Compounds, Russian Academy of Sciences 2. Belgorod State University
Abstract
Alzheimer’s disease (AD) is the most common proteinopathy, which is accompanied by a steady decrease in the patient’s cognitive functions with simultaneous accumulation of extracellular aggregates of amyloid β (Aβ) – amyloid plaques in the brain tissues and associated with neuroinflammation and neurodegeneration. Unlike humans and all other mammals, rats and mice have three amino acid substitutions in Aβ and do not reproduce the Alzheimer’s pathology. However, the appearance of amyloid plaques is observed in the brains of transgenic mice with the overexpression of human Aβ, which makes it possible to widely use these transgenic animals in biomedicine for the manifestation of AD. Transgenic mouse line APPswe/PS1dE9 is a widely used animal model for the study of the molecular mechanisms of AD. In this paper we provide a detailed description of the APPswe/PS1dE9/Blg subline of animals obtained by crossing APPswe/PS1dE9 mice on a CH3 genetic background with C57Bl6/Chg animals. We have shown no difference in parameters of offspring’s survival and fertility of this line compared to wild-type control animals. Histological analysis of the brain of APPswe/PS1dE9/Blg line confirmed the main neuromorphological feature of AD with the progression in number and size of amyloid plaques during aging. Thus, APPswe/PS1dE9/Blg line is a convenient model in the search for therapeutic strategies for AD.
Publisher
The Russian Academy of Sciences
Reference38 articles.
1. Konttinen H., Cabral-da-Silva M.E.C., Ohtonen S., Wojciechowski S., Shakirzyanova A., Caligola S., Giugno R., Ishchenko Y., Hernandez D., Fazaludeen M.F., Eamen S., Budia M.G., Fagerlund I., Scoyni F., Korhonen P., Huber N., Haapasalo A., Hewitt A.W., Vickers J., Smith G.C., Oksanen M., Graff C., Kanninen K.M., Lehtonen S., Propson N., Schwartz M.P., Pebay A., Koistinaho J., Ooi L., Malm T. (2019) PSEN1DeltaE9, APPswe, and APOE4 confer disparate phenotypes in human iPSC-derived microglia. Stem. Cell Rep. 13, 669–683. 2. Шелковникова Т.А., Куликова А.А., Цветков Ф.О., Peters O., Бачурин С.О., Бухман В.Л., Нинкина Н.Н. (2012) Протеинопатии – формы нейродегенеративных заболеваний, в основе которых лежит патологическая агрегация белков. Молекуляр. биология. 46, 402–415. 3. Masters C.L., Bateman R., Blennow K., Rowe C.C., Sperling R.A., Cummings J.L. (2015) Alzheimer’s disease. Nat. Rev. Dis. Primers. 1, 15056. 4. Kozin S.A., Cheglakov I.B., Ovsepyan A.A., Telegin G.B., Tsvetkov P.O., Lisitsa A.V., Makarov A.A. (2013) Peripherally applied synthetic peptide isoAsp7-Abeta(1-42) triggers cerebral beta-amyloidosis. Neurotoxicity Res. 24, 370–376. 5. Evin G., Li Q.X. (2012) Platelets and Alzheimer’s disease: potential of APP as a biomarker. W. J. Psychiatry. 2, 102–113.
Cited by
2 articles.
订阅此论文施引文献
订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献
|
|