Source:http://linkedlifedata.com/resource/pubmed/id/15158161
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rdf:type | |
lifeskim:mentions |
umls-concept:C0002395,
umls-concept:C0006104,
umls-concept:C0017262,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0086418,
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umls-concept:C0596988,
umls-concept:C0917874,
umls-concept:C0936012,
umls-concept:C1171362,
umls-concept:C1364818,
umls-concept:C1515670,
umls-concept:C1533134,
umls-concept:C1979963,
umls-concept:C2003903
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pubmed:issue |
1-2
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pubmed:dateCreated |
2004-5-25
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pubmed:abstractText |
Transgenic mice that express mutant human amyloid precursor protein (APPTg2576) develop beta-amyloid (Abeta) plaques throughout the cortex starting at 10-12 months of age. We examined the neurochemical profile of APPTg2576 mice using in vitro and in vivo magnetic resonance spectroscopy (MRS); gross abnormalities using magnetic resonance imaging (MRI) and plaque distribution; size and number using immunohistochemistry. Transgenic mice were anesthetized with halothane and scanned at 4.7 T using T2-weighted imaging and in vivo MRS of frontal cortex. In vitro MRS was run from brain extracts of frontal cortex in both APP and wild-type mice. Mice were also perfused and brains were collected and cut for immunohistochemistry. We found that N-acetylaspartate (NAA), glutamate and glutathione were decreased by 17%, 22% and 36%, respectively, in the cerebral cortex of APP transgenic mice at 19 months of age when Abeta deposits are widespread. Taurine was increased 21% compared to wild-type. Decreased levels of NAA and increased levels of taurine are consistent with decreased neuronal viability and increased glial volume, and are similar to findings of decreased NAA and increased myo-inositol in human Alzheimer's disease (AD) brains. Correlation between the severity of Abeta deposition and altered neurochemical profile remains to be studied. Nevertheless, the altered neurochemical profile may be a valuable marker to test therapeutics in this mouse model.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2004 Elsevier B.V.
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pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
1012
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
60-5
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15158161-Alzheimer Disease,
pubmed-meshheading:15158161-Amyloid beta-Protein Precursor,
pubmed-meshheading:15158161-Animals,
pubmed-meshheading:15158161-Brain,
pubmed-meshheading:15158161-Gene Expression Regulation,
pubmed-meshheading:15158161-Humans,
pubmed-meshheading:15158161-Magnetic Resonance Spectroscopy,
pubmed-meshheading:15158161-Mice,
pubmed-meshheading:15158161-Mice, Transgenic
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pubmed:year |
2004
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pubmed:articleTitle |
Magnetic resonance spectroscopic analysis of Alzheimer's disease mouse brain that express mutant human APP shows altered neurochemical profile.
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pubmed:affiliation |
Geriatric Research Education and Clinical Center, Bedford Veterans Administration Medical Center, MA 01730, USA. dedeoglu@bu.edu
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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