当前位置： SCI文献检索 > CELLULAR AND MOLECULAR NEUROBIOLOGY期刊下所有文献 > Early changes in behavior deficits, amyloid beta-42 deposits and MAPK activation in doubly transgenic mice co-expressing NSE-controlled human mutant PS2 and APPsw.

Early changes in behavior deficits, amyloid beta-42 deposits and MAPK activation in doubly transgenic mice co-expressing NSE-controlled human mutant PS2 and APPsw.

Abstract：

:1. Doubly transgenic mice were some differences in the period proceeding of the development of Abeta-42 deposits and behavioral deficits. It was not characterized human mutant PS2 (hPS2) with APPsw in the brains of double transgenic mice. The aim of this study was to examine whether doubly transgenic mice co-expressing NSE-controlled APPsw and hPS2m develop AD-like phenotypes much earlier than singly APPsw or hPS2m alone. 2. We produced doubly transgenic mice from a cross between our previously created NSE-controlled hPS2m and an APPsw transgenic line. This doubly transgenic line was quantitatively produced by cross with age-matched control mice, and the produced mice were separated into 5, 6, 7 and 8-month old age groups. At the age of 8 months, the four groups of mice were tested for behavioral function, levels of Abeta-42 deposition, and potential signaling events. 3. It was shown that all the AD-like phenotypes, including behavior deficits, Abeta-42 levels, MAPK activation and ER expressions in doubly transgenic mice develop much earlier in the early time of AD development than their singly transgenic and non-transgenic littermates. 4. The results suggest that elevated Abeta-42 levels, and MAPK activation in doubly transgenic mice are model for early diagnosis and treatment of AD with therapeutic drug.

journal_name

Cell Mol Neurobiol

journal_title

Cellular and molecular neurobiology

authors

Hwang DY,Cho JS,Oh JH,Shim SB,Jee SW,Lee SH,Seo SJ,Song CW,Lee SH,Kim YK

doi

10.1007/s10571-005-4950-x

subject

Has Abstract

pub_date

2005-08-01 00:00:00

pages

881-98

issue

5

eissn

0272-4340

issn

1573-6830

journal_volume

25

pub_type

杂志文章

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