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Normal cognitive behavior in two distinct congenic lines of transgenic mice hyperexpressing mutant APPSWE

Savonenko, Alena V, Xu, Guilian M, Price, Donald L, Borchelt, David R, Markowska, Alicja L·2003·Neurobiology of Disease
DOI 10.1016/s0969-9961(02)00012-8
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Abstract

Amyloid deposition appears to be an early and crucial event in Alzheimer's disease (AD). To generate animal models of AD, mice expressing full-length amyloid precursor protein (APP), with mutations linked to FAD, have been created. These animals exhibit abnormalities characteristic of AD, including deposits of beta-amyloid (Abeta), neuritic plaques, and glial responses. In studies of cognition in these animals, there have been several reports of memory disturbances well before the appearance of amyloid deposits. We have developed two distinct lines of transgenic mice (C3-3 and E1-2) that express the "Swedish" variant of APP (APP(SWE)) at levels that are approximately three-fold higher than endogenous mouse APP. Both lines have been backcrossed to C57BL/6J mice for 10 generations. Here, we use longitudinal and cross-sectional studies to evaluate the cognitive performance of our animals, where the concentration of Abeta1-42 in brain increases with aging from low levels (2-10 pmol/g) at 6-14 months of age to relatively high levels (60-100 pmol/g) at 24-26 months, when deposits of Abeta were beginning to form. When 12-month-old mice were tested in tasks that assess reference and working memory, transgenic mice from both lines could not be distinguished from nontransgenic littermates. Further study of 24- to 26-month-old transgenic mice (C3-3 line) found no evidence of memory impairment despite the presence of high levels of human Abeta (60-100 pmol/g). Thus, the expression of APP…

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  • Transfer of the APPswe and mutant PS1 transgene from the hybrid background to C57BL/6J mice modestly delays the onset of amyloid deposition to lower amyloid loads at younger ages.

    “In prior studies of mice that harbor the APPswe and mutant PS1 transgene constructs utilized here, we have noted that transfer of the transgene from the hybrid background to C57BL/6J mice modestly delays the onset of amyloid deposition to lower amyloid loads at younger ages [34].”

    From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [34]

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Metadata

Authors
Savonenko, A. V., Xu, G. M., Price, D. L., Borchelt, D. R., & Markowska, A. L.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2003-04
Volume
12
Issue
3
Pages
194-211
ISSN
0969-9961
DOI
10.1016/s0969-9961(02)00012-8
Cited by
63
References
8
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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