Source:http://linkedlifedata.com/resource/pubmed/id/15312961
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2004-8-17
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pubmed:abstractText |
Biochemical and genetic studies indicate that the inflammatory proteins, apolipoprotein E (ApoE) and alpha(1)-antichymotrypsin (ACT) are important in the pathogenesis of Alzheimer's disease (AD). Using several lines of multiply transgenic/knockout mice we show here that murine ApoE and human ACT separately and synergistically facilitate both diffuse A beta immunoreactive and fibrillar amyloid deposition and thus also promote cognitive impairment in aged PDAPP(V717F) mice. The degree of cognitive impairment is highly correlated with the ApoE- and ACT-dependent hippocampal amyloid burden, with PDAPP mice lacking ApoE and ACT having little amyloid and little learning disability. A analysis of young mice before the onset of amyloid formation shows that steady-state levels of monomeric A beta peptide are unchanged by ApoE or ACT. These data suggest that the process or product of amyloid formation is more critical than monomeric A beta for the neurological decline in AD, and that the risk factors ApoE and ACT participate primarily in disease processes downstream of APP processing.
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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 |
Oct
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pubmed:issn |
0197-4580
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pubmed:author |
pubmed-author:ArendashGary WGW,
pubmed-author:BalesKelly RKR,
pubmed-author:CostaDavid ADA,
pubmed-author:CraccioloJennifer RJR,
pubmed-author:GarciaMarcos FMF,
pubmed-author:LeightyRalph ERE,
pubmed-author:LowMark AMA,
pubmed-author:NilssonLars N GLN,
pubmed-author:PaulSteven MSM,
pubmed-author:PotterHuntingtonH,
pubmed-author:RojianiAmynA,
pubmed-author:WuXinX
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pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1153-67
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:15312961-Aging,
pubmed-meshheading:15312961-Alzheimer Disease,
pubmed-meshheading:15312961-Amyloid beta-Peptides,
pubmed-meshheading:15312961-Animals,
pubmed-meshheading:15312961-Apolipoproteins E,
pubmed-meshheading:15312961-Brain,
pubmed-meshheading:15312961-Cognition Disorders,
pubmed-meshheading:15312961-Disease Models, Animal,
pubmed-meshheading:15312961-Encephalitis,
pubmed-meshheading:15312961-Female,
pubmed-meshheading:15312961-Hippocampus,
pubmed-meshheading:15312961-Learning Disorders,
pubmed-meshheading:15312961-Male,
pubmed-meshheading:15312961-Maze Learning,
pubmed-meshheading:15312961-Mice,
pubmed-meshheading:15312961-Mice, Knockout,
pubmed-meshheading:15312961-Mice, Transgenic,
pubmed-meshheading:15312961-Plaque, Amyloid,
pubmed-meshheading:15312961-alpha 1-Antichymotrypsin
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pubmed:year |
2004
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pubmed:articleTitle |
Cognitive impairment in PDAPP mice depends on ApoE and ACT-catalyzed amyloid formation.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, Suncoast Gerontology Center, University of South Florida, 12901 Bruce B. Downs Blvd., Tampa, FL 33612, USA.
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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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