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NSE-controlled carboxyl-terminus of APP gene over-expressing in transgenic mice induces altered expressions in behavior, Aβ-42, and GSK3β binding proteins

Title
NSE-controlled carboxyl-terminus of APP gene over-expressing in transgenic mice induces altered expressions in behavior, Aβ-42, and GSK3β binding proteins
Authors
Lim H.J.Cho J.S.Oh J.H.Shim S.B.Hwang D.Y.Jee S.W.Lee S.H.Sheen Y.Y.Kim Y.K.
Ewha Authors
신윤용
SCOPUS Author ID
신윤용scopus
Issue Date
2005
Journal Title
Cellular and Molecular Neurobiology
ISSN
0272-4340JCR Link
Citation
vol. 25, no. 5, pp. 833 - 850
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The amyloid protein precursor (APP) is cleaved in its intramembranous domain by γ-secrease to generate amyloid β and a free carboxyl-terminal intracellular fragment. The carboxyl-terminal of 105 amino acids of APP (APP-C105) plays a crucial role in the neuropathology of Alzheimer's disease (AD), but it is incompletely understand how APP-C105 overexpression interacts and regulates the brain function and Aβ-42 levels, and whether or not it is associated with the expressions of GSK3β-binding proteins. To test this, transgenic mice expressing NSE-controlled APP-C105 were produced and tested for their above phenotypes. A behavioral deficit was observed in the 9 months old transgenic mice, and western blot indicated that there was a predominant expression of APP-C105 in transgenic brains compared with those of non-transgenic brains. In parallel, APP-C105 overexpression resulted in the modulation of the Aβ-42 level, γ-secretase activity, GSK3β-binding proteins including PS1, tau, and β-catenin in the brains of the transgenic mice relative to the non-transgenic mice. Thus, altered expressions of these neuropathological phenotypes in APP-C105 transgenic mice could be useful targets in developing new therapeutic treatments. © 2005 Springer Science+Business Media, Inc.
DOI
10.1007/s10571-005-4937-7
Appears in Collections:
약학대학 > 약학과 > Journal papers
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