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

Singer, Oded, Marr, Robert A, Rockenstein, Edward, Crews, Leslie, Coufal, Nicole G, Gage, Fred H, Verma, Inder M, Masliah, Eliezer·2005·Nature Neuroscience

DOI 10.1038/nn1531

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Phospho-eIF2α Level Is Important for Determining Abilities of BACE1 Reduction to Rescue Cholinergic Neurodegeneration and Memory Defects in 5XFAD Mice
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“Emerging evidence suggests that partial reduction of BACE1, which is induced by BACE1 gene deletion [21,22], siRNA targeting BACE1 [18] and immunization with BACE1 ectodomain [19], can diminish brain Ab levels and amyloid-related”
Background
MT5-MMP is a new pro-amyloidogenic proteinase that promotes amyloid pathology and cognitive decline in a transgenic mouse model of Alzheimer’s disease
Baranger, K., Marchalant, Y., Bonnet, A. E., Crouzin, N., Carrete, A., Paumier, J.-M., Py, N. A., Bernard, A., Bauer, C., Charrat, E., et al. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-015-1992-1 · Cited by 133
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“In fact, several studies unequivocally demonstrated that inhibition of BACE1 by RNAi-mediated knock-down or genetic deletion ameliorates Ab-associated pathologies and cognitive deficits in mouse models of Ab-amyloidosis (Luo et al. 2001; Ohno et al. 2004; Laird et al. 2005; Singer et al. 2005; McConlogue et al. 2007).”
BackgroundInfluential
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The effect of BACE1-AS on β-amyloid generation by regulating BACE1 mRNA expression
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Polymers for the treatment of Alzheimer’s disease
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Untitled work
(2015) · Europe PMC (PubMed Central)

Authors: Singer, O., Marr, R. A., Rockenstein, E., Crews, L., Coufal, N. G., Gage, F. H., Verma, I. M., & Masliah, E.
Venue: Nature Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2005-08-28
Volume: 8
Issue: 10
Pages: 1343-1349
ISSN: 1097-6256 (ISSN-L)
1546-1726
DOI: 10.1038/nn1531
OpenAlex: W2160678872
Cited by: 428
References: 6
FWCI: 19.16
Type: journal article
Language: en
Open access: closed

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

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