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Müller, U; Cristina, N; Li, Z W; Wolfer, D P; Lipp, H P; Rülicke, T; Brandner, S; Aguzzi, A; Weissman, C (1996). Mice homozygous for a modified beta-amyloid precursor protein (beta APP) gene show impaired behavior and high incidence of agenesis of the corpus callosum. Annals of the New York Academy of Sciences, 777:65-73.

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Abstract

The amyloid precursor protein (beta APP) gene of the mouse was disrupted by homologous recombination; however, contrary to expectation, brain and other tissues still contained beta APP-specific RNA, albeit at a level 5-10 fold lower than wild-type and lacking the disrupted exon, which had been spliced out. The brain contained shortened beta APP-specific protein at a low level. Mutant mice were severely impaired in spatial learning and exploratory behavior and showed increased incidence of agenesis of the corpus callosum.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:1996
Deposited On:11 Feb 2008 12:25
Last Modified:28 Nov 2013 02:13
Publisher:Wiley-Blackwell
ISSN:0077-8923
Publisher DOI:10.1111/j.1749-6632.1996.tb34402.x
PubMed ID:8624128
Citations:Web of Science®. Times Cited: 5
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