• Cell. Mol. Neurobiol. · Aug 2005

    NSE-controlled carboxyl-terminus of APP gene over-expressing in transgenic mice induces altered expressions in behavior, Abeta-42, and GSK3beta binding proteins.

    • Hwa J Lim, Jung S Cho, Jae H Oh, Sun B Shim, Dae Y Hwang, Seung W Jee, Su H Lee, Yhun Y Sheen, Seok H Lee, and Yong K Kim.
    • Division of Laboratory Animal Resources, Korea Food and Drug Administration, National Institute of Toxicological Research, 5 Nokbun-dong Eunpyng-ku, Seoul 122-704, Republic of Korea.
    • Cell. Mol. Neurobiol. 2005 Aug 1; 25 (5): 833-50.

    AbstractThe amyloid protein precursor (APP) is cleaved in its intramembranous domain by gamma-secrease to generate amyloid beta 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 Abeta-42 levels, and whether or not it is associated with the expressions of GSK3beta-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 Abeta-42 level, gamma-secretase activity, GSK3beta-binding proteins including PS1, tau, and beta-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.

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