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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2005-9-28
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pubmed:databankReference |
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pubmed:abstractText |
In Alzheimer disease, increased beta-secretase (BACE1) activity has been associated with neurodegeneration and accumulation of amyloid precursor protein (APP) products. Thus, inactivation of BACE1 could be important in the treatment of Alzheimer disease. In this study, we found that lowering BACE1 levels using lentiviral vectors expressing siRNAs targeting BACE1 reduced amyloid production and the neurodegenerative and behavioral deficits in APP transgenic mice, a model of Alzheimer disease. Our results suggest that lentiviral vector delivery of BACE1 siRNA can specifically reduce the cleavage of APP and neurodegeneration in vivo and indicate that this approach could have potential therapeutic value for treatment of Alzheimer disease.
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pubmed:grant |
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid Precursor Protein Secretases,
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Protein Precursor,
http://linkedlifedata.com/resource/pubmed/chemical/Aspartic Acid Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/BACE1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Bace1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/Glial Fibrillary Acidic Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Microtubule-Associated Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mtap2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1097-6256
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1343-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16136043-Alzheimer Disease,
pubmed-meshheading:16136043-Amyloid Precursor Protein Secretases,
pubmed-meshheading:16136043-Amyloid beta-Protein Precursor,
pubmed-meshheading:16136043-Analysis of Variance,
pubmed-meshheading:16136043-Animals,
pubmed-meshheading:16136043-Aspartic Acid Endopeptidases,
pubmed-meshheading:16136043-Brain,
pubmed-meshheading:16136043-Cell Line,
pubmed-meshheading:16136043-Cloning, Molecular,
pubmed-meshheading:16136043-Disease Models, Animal,
pubmed-meshheading:16136043-Endopeptidases,
pubmed-meshheading:16136043-Gene Expression Regulation,
pubmed-meshheading:16136043-Genetic Vectors,
pubmed-meshheading:16136043-Glial Fibrillary Acidic Protein,
pubmed-meshheading:16136043-Humans,
pubmed-meshheading:16136043-Immunohistochemistry,
pubmed-meshheading:16136043-Lentivirus,
pubmed-meshheading:16136043-Maze Learning,
pubmed-meshheading:16136043-Mice,
pubmed-meshheading:16136043-Mice, Transgenic,
pubmed-meshheading:16136043-Microtubule-Associated Proteins,
pubmed-meshheading:16136043-Molecular Sequence Data,
pubmed-meshheading:16136043-RNA, Small Interfering,
pubmed-meshheading:16136043-Spatial Behavior,
pubmed-meshheading:16136043-Time Factors
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pubmed:year |
2005
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pubmed:articleTitle |
Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model.
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pubmed:affiliation |
Laboratory of Genetics, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, 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,
Research Support, N.I.H., Extramural
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