pubmed-article:9427614 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C0282641 | lld:lifeskim |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C0085151 | lld:lifeskim |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C0299212 | lld:lifeskim |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C1418985 | lld:lifeskim |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
pubmed-article:9427614 | lifeskim:mentions | umls-concept:C0206243 | lld:lifeskim |
pubmed-article:9427614 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:9427614 | pubmed:dateCreated | 1998-1-23 | lld:pubmed |
pubmed-article:9427614 | pubmed:abstractText | Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. The mutant APP(K670N,M671L) transgenic line, Tg2576, shows markedly elevated amyloid beta-protein (A beta) levels at an early age and, by 9-12 months, develops extracellular AD-type A beta deposits in the cortex and hippocampus. Mutant PS1 transgenic mice do not show abnormal pathology, but do display subtly elevated levels of the highly amyloidogenic 42- or 43-amino acid peptide A beta42(43). Here we demonstrate that the doubly transgenic progeny from a cross between line Tg2576 and a mutant PS1M146L transgenic line develop large numbers of fibrillar A beta deposits in cerebral cortex and hippocampus far earlier than their singly transgenic Tg2576 littermates. In the period preceding overt A beta deposition, the doubly transgenic mice show a selective 41% increase in A beta42(43) in their brains. Thus, the development of AD-like pathology is substantially enhanced when a PS1 mutation, which causes a modest increase in A beta42(43), is introduced into Tg2576-derived mice. Remarkably, both doubly and singly transgenic mice showed reduced spontaneous alternation performance in a "Y" maze before substantial A beta deposition was apparent. This suggests that some aspects of the behavioral phenotype in these mice may be related to an event that precedes plaque formation. | lld:pubmed |
pubmed-article:9427614 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:language | eng | lld:pubmed |
pubmed-article:9427614 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9427614 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9427614 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9427614 | pubmed:month | Jan | lld:pubmed |
pubmed-article:9427614 | pubmed:issn | 1078-8956 | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:MorganDD | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:HardyJJ | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:SandersSS | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:WrightKK | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:MuellerRR | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:McGowanEE | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:GordonM NMN | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:YuXX | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:DuffKK | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:HsiaoKK | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:HolcombLL | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:BenkovicSS | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:SaadII | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:YounkinSS | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:JantzenPP | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:EckmanCC | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:PradaC MCM | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:ZehrCC | lld:pubmed |
pubmed-article:9427614 | pubmed:author | pubmed-author:O'CampoKK | lld:pubmed |
pubmed-article:9427614 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9427614 | pubmed:volume | 4 | lld:pubmed |
pubmed-article:9427614 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9427614 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9427614 | pubmed:pagination | 97-100 | lld:pubmed |
pubmed-article:9427614 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:9427614 | pubmed:meshHeading | pubmed-meshheading:9427614-... | lld:pubmed |
pubmed-article:9427614 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9427614 | pubmed:articleTitle | Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes. | lld:pubmed |
pubmed-article:9427614 | pubmed:affiliation | Department of Pharmacology, University of South Florida, Tampa 33612, USA. | lld:pubmed |
pubmed-article:9427614 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9427614 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:9427614 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9427614 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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