| pubmed-article:8744401 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8744401 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:8744401 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:8744401 | lifeskim:mentions | umls-concept:C0276496 | lld:lifeskim |
| pubmed-article:8744401 | lifeskim:mentions | umls-concept:C0599155 | lld:lifeskim |
| pubmed-article:8744401 | lifeskim:mentions | umls-concept:C0205251 | lld:lifeskim |
| pubmed-article:8744401 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8744401 | pubmed:dateCreated | 1996-10-24 | lld:pubmed |
| pubmed-article:8744401 | pubmed:abstractText | Point mutations within the beta-amyloid precusor protein (beta-APP) gene known to segregate with Alzheimer's disease in certain families were introduced into human beta-APP cDNAs and expressed under the control of a neuron-specific enolase (NSE) promoter in mice. The transgenic animals exhibited transgene expression predominantly in neocortex and hippocampus where the levels were maximally 1.3-fold of those of wild-type mouse beta-APP. Quantitative immunoblot analysis in homozygous mice carrying different missense mutations showed slightly increased alpha-secretory processing. In V7171 mice compared to nontransgenic mice there was more alpha-secretory beta-APP (beta-APPsec) in cortex/hippocampus, less in cerebellum, and no difference in midbrain/brain stem. In none of the transgenic animals tested was a 4 kDa amyloid fragment detected by Western blotting of brain extracts, immunohistochemistry, or by 125I-A beta-binding onto brain sections. No glial reaction was observed. Behavioral analysis of mice carrying the V7171 mutation showed no appreciable deficit in comparison to wild-type mice. Together, these data suggest that low levels of expression of mutated beta-APP in 10-12-month-old transgenic mouse brains result in slightly more beta-APPsec, and are insufficient to induce amyloidogenic processing and AD-like pathology. | lld:pubmed |
| pubmed-article:8744401 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8744401 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8744401 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8744401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8744401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8744401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8744401 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8744401 | pubmed:issn | 0197-4580 | lld:pubmed |
| pubmed-article:8744401 | pubmed:author | pubmed-author:HuberGG | lld:pubmed |
| pubmed-article:8744401 | pubmed:author | pubmed-author:RichardsJ GJG | lld:pubmed |
| pubmed-article:8744401 | pubmed:author | pubmed-author:MartinJ RJR | lld:pubmed |
| pubmed-article:8744401 | pubmed:author | pubmed-author:MaggioJJ | lld:pubmed |
| pubmed-article:8744401 | pubmed:author | pubmed-author:MalherbePP | lld:pubmed |
| pubmed-article:8744401 | pubmed:author | pubmed-author:BluethmannHH | lld:pubmed |
| pubmed-article:8744401 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8744401 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:8744401 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8744401 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8744401 | pubmed:pagination | 205-14 | lld:pubmed |
| pubmed-article:8744401 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
| pubmed-article:8744401 | pubmed:meshHeading | pubmed-meshheading:8744401-... | lld:pubmed |
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| pubmed-article:8744401 | pubmed:meshHeading | pubmed-meshheading:8744401-... | lld:pubmed |
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| pubmed-article:8744401 | pubmed:meshHeading | pubmed-meshheading:8744401-... | lld:pubmed |
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| pubmed-article:8744401 | pubmed:meshHeading | pubmed-meshheading:8744401-... | lld:pubmed |
| pubmed-article:8744401 | pubmed:articleTitle | Lack of beta-amyloidosis in transgenic mice expressing low levels of familial Alzheimer's disease missense mutations. | lld:pubmed |
| pubmed-article:8744401 | pubmed:affiliation | Pharma Division, F. Hoffmann-La Roche Ltd., Basel, Switzerland. | lld:pubmed |
| pubmed-article:8744401 | pubmed:publicationType | Journal Article | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8744401 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8744401 | lld:pubmed |
