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Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein
- Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein
- 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
- SCOPUS Author ID
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- Journal Title
- Neurobiology of Disease
- Neurobiology of Disease vol. 22, no. 1, pp. 10 - 24
- SCIE; SCOPUS
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- 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.
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