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Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein

Title
Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein
Authors
Lee K.-W.Im J.-Y.Song J.-S.Lee S.H.Lee H.-J.Ha H.-Y.Koh J.-Y.Gwag B.J.Yang S.-D.Paik S.-G.Han P.-L.
Ewha Authors
한평림
SCOPUS Author ID
한평림scopus
Issue Date
2006
Journal Title
Neurobiology of Disease
ISSN
0969-9961JCR Link
Citation
vol. 22, no. 1, pp. 10 - 24
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The β-secretase cleaved Aβ-bearing carboxy-terminal fragments (βCTFs) of amyloid precursor protein (APP) in neural cells have been suggested to be cytotoxic. However, the functional significance of βCTFs in vivo remains elusive. We created a transgenic mouse line Tg-βCTF99/B6 expressing the human βCTF99 in the brain of inbred C57BL/6 strain. Tg-βCTF99/B6 mouse brain at 12-16 months showed severely down-regulated calbindin, phospho-CREB, and Bcl-xL expression and up-regulated phospho-JNK, Bcl-2, and Bax expression. Neuronal cell density in the Tg-βCTF99/B6 cerebral cortex at 16-18 months was lower than that of the non-transgenic control, but not at 5 months. At 11-14 months, Tg-βCTF99/B6 mice displayed cognitive impairments and increased anxiety, which were not observed at 5 months. These results suggest that increased βCTF99 expression is highly detrimental to the aging brain and that it produces a progressive and age-dependent AD-like pathogenesis. © 2005 Elsevier Inc. All rights reserved.
DOI
10.1016/j.nbd.2005.09.011
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일반대학원 > 뇌·인지과학과 > Journal papers
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