Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-10

AUTHORS

Oded Singer, Robert A Marr, Edward Rockenstein, Leslie Crews, Nicole G Coufal, Fred H Gage, Inder M Verma, Eliezer Masliah

ABSTRACT

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. More... »

PAGES

1343-1349

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nn1531

DOI

http://dx.doi.org/10.1038/nn1531

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008434335

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16136043


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