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rdf:type |
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lifeskim:mentions |
umls-concept:C0003069,
umls-concept:C0004927,
umls-concept:C0026809,
umls-concept:C0085151,
umls-concept:C0205329,
umls-concept:C0596260,
umls-concept:C0684336,
umls-concept:C1512692,
umls-concept:C1521751,
umls-concept:C1555903,
umls-concept:C1850496,
umls-concept:C2598156
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pubmed:issue |
1
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pubmed:dateCreated |
2006-3-27
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pubmed:abstractText |
The beta-secretase cleaved Abeta-bearing carboxy-terminal fragments (betaCTFs) of amyloid precursor protein (APP) in neural cells have been suggested to be cytotoxic. However, the functional significance of betaCTFs in vivo remains elusive. We created a transgenic mouse line Tg-betaCTF99/B6 expressing the human betaCTF99 in the brain of inbred C57BL/6 strain. Tg-betaCTF99/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-betaCTF99/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-betaCTF99/B6 mice displayed cognitive impairments and increased anxiety, which were not observed at 5 months. These results suggest that increased betaCTF99 expression is highly detrimental to the aging brain and that it produces a progressive and age-dependent AD-like pathogenesis.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0969-9961
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pubmed:author |
pubmed-author:GwagByoung JooBJ,
pubmed-author:HaHye-YeongHY,
pubmed-author:HanPyung-LimPL,
pubmed-author:ImJoo-YoungJY,
pubmed-author:KohJae-YoungJY,
pubmed-author:LeeHo-JeongHJ,
pubmed-author:LeeKang-WooKW,
pubmed-author:LeeSi HyoungSH,
pubmed-author:PaikSang-GiSG,
pubmed-author:SongJin-SookJS,
pubmed-author:YangSung-DonSD
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pubmed:issnType |
Print
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
10-24
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:16289866-Aging,
pubmed-meshheading:16289866-Alzheimer Disease,
pubmed-meshheading:16289866-Amyloid beta-Peptides,
pubmed-meshheading:16289866-Amyloid beta-Protein Precursor,
pubmed-meshheading:16289866-Animals,
pubmed-meshheading:16289866-Anxiety Disorders,
pubmed-meshheading:16289866-Apoptosis,
pubmed-meshheading:16289866-Behavioral Symptoms,
pubmed-meshheading:16289866-Brain,
pubmed-meshheading:16289866-Cell Line,
pubmed-meshheading:16289866-Cognition Disorders,
pubmed-meshheading:16289866-Disease Models, Animal,
pubmed-meshheading:16289866-Disease Progression,
pubmed-meshheading:16289866-Down-Regulation,
pubmed-meshheading:16289866-Mice,
pubmed-meshheading:16289866-Mice, Inbred C57BL,
pubmed-meshheading:16289866-Mice, Transgenic,
pubmed-meshheading:16289866-Nerve Degeneration,
pubmed-meshheading:16289866-Nerve Tissue Proteins,
pubmed-meshheading:16289866-Peptide Fragments,
pubmed-meshheading:16289866-Protein Structure, Tertiary,
pubmed-meshheading:16289866-Signal Transduction,
pubmed-meshheading:16289866-Up-Regulation
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pubmed:year |
2006
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pubmed:articleTitle |
Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein.
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pubmed:affiliation |
Department of Neuroscience, Neuroscience Research Center and Medical Research Institute, Ewha Womans University School of Medicine, 911-1 Mok-6-Dong, Yangchun-Gu, Seoul 158-710, South Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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