Mice expressing human mutant presenilin-1 exhibit decreased activation of NF-κB p50 in hippocampal neurons after injury

C. A. Kassed; T. L. Butler; M. T. Navidomskis; M. N. Gordon; D. Morgan; K. R. Pennypacker

doi:10.1016/S0169-328X(02)00658-7

Mice expressing human mutant presenilin-1 exhibit decreased activation of NF-κB p50 in hippocampal neurons after injury

C. A. Kassed, T. L. Butler, M. T. Navidomskis, M. N. Gordon, D. Morgan, K. R. Pennypacker

Research output: Contribution to journal › Article › peer-review

24 Citations (SciVal)

Abstract

Mutations in the presenilin-1 (mutPS-1) gene, a cause of familial Alzheimer's disease, increase the susceptibility of neurons to apoptotic death. Using the trimethyltin model of hippocampal neurodegeneration, mice expressing the human mutPS-1 gene (M146L) exhibited increased neurodegeneration and mortality relative to non-transgenic littermates. Activation of NF-κB p50 was found to be impaired in transgenic mice with unaltered expression levels suggesting that mutPS-1 expression inhibits p50 activation to adversely affect neuronal resistance to injury.

Original language	English
Pages (from-to)	152-157
Number of pages	6
Journal	Molecular Brain Research
Volume	110
Issue number	1
DOIs	https://doi.org/10.1016/S0169-328X(02)00658-7
State	Published - Jan 31 2003

Bibliographical note

Funding Information:
This research was supported by NIH Grant RO1 NS39141-01A2 and American Heart Association Grants 9930072N (K.R.P.) and 0120233B (T.L.B.).

Keywords

Fluoro-Jade
Hippocampus
NF-κB
Neurodegeneration
Neuroprotection
Neurotoxicity
P50
Presenilin-1 gene mutations
Resistance to injury
Signal transduction
Transcription factors
Trimethyltin
mutPS-1 mice

ASJC Scopus subject areas

Molecular Biology
Cellular and Molecular Neuroscience

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0169-328X(02)00658-7

Cite this

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title = "Mice expressing human mutant presenilin-1 exhibit decreased activation of NF-κB p50 in hippocampal neurons after injury",

abstract = "Mutations in the presenilin-1 (mutPS-1) gene, a cause of familial Alzheimer's disease, increase the susceptibility of neurons to apoptotic death. Using the trimethyltin model of hippocampal neurodegeneration, mice expressing the human mutPS-1 gene (M146L) exhibited increased neurodegeneration and mortality relative to non-transgenic littermates. Activation of NF-κB p50 was found to be impaired in transgenic mice with unaltered expression levels suggesting that mutPS-1 expression inhibits p50 activation to adversely affect neuronal resistance to injury.",

keywords = "Fluoro-Jade, Hippocampus, NF-κB, Neurodegeneration, Neuroprotection, Neurotoxicity, P50, Presenilin-1 gene mutations, Resistance to injury, Signal transduction, Transcription factors, Trimethyltin, mutPS-1 mice",

author = "Kassed, {C. A.} and Butler, {T. L.} and Navidomskis, {M. T.} and Gordon, {M. N.} and D. Morgan and Pennypacker, {K. R.}",

note = "Funding Information: This research was supported by NIH Grant RO1 NS39141-01A2 and American Heart Association Grants 9930072N (K.R.P.) and 0120233B (T.L.B.). ",

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T1 - Mice expressing human mutant presenilin-1 exhibit decreased activation of NF-κB p50 in hippocampal neurons after injury

AU - Kassed, C. A.

AU - Butler, T. L.

AU - Navidomskis, M. T.

AU - Gordon, M. N.

AU - Morgan, D.

AU - Pennypacker, K. R.

N1 - Funding Information: This research was supported by NIH Grant RO1 NS39141-01A2 and American Heart Association Grants 9930072N (K.R.P.) and 0120233B (T.L.B.).

PY - 2003/1/31

Y1 - 2003/1/31

N2 - Mutations in the presenilin-1 (mutPS-1) gene, a cause of familial Alzheimer's disease, increase the susceptibility of neurons to apoptotic death. Using the trimethyltin model of hippocampal neurodegeneration, mice expressing the human mutPS-1 gene (M146L) exhibited increased neurodegeneration and mortality relative to non-transgenic littermates. Activation of NF-κB p50 was found to be impaired in transgenic mice with unaltered expression levels suggesting that mutPS-1 expression inhibits p50 activation to adversely affect neuronal resistance to injury.

AB - Mutations in the presenilin-1 (mutPS-1) gene, a cause of familial Alzheimer's disease, increase the susceptibility of neurons to apoptotic death. Using the trimethyltin model of hippocampal neurodegeneration, mice expressing the human mutPS-1 gene (M146L) exhibited increased neurodegeneration and mortality relative to non-transgenic littermates. Activation of NF-κB p50 was found to be impaired in transgenic mice with unaltered expression levels suggesting that mutPS-1 expression inhibits p50 activation to adversely affect neuronal resistance to injury.

KW - Fluoro-Jade

KW - Hippocampus

KW - NF-κB

KW - Neurodegeneration

KW - Neuroprotection

KW - Neurotoxicity

KW - P50

KW - Presenilin-1 gene mutations

KW - Resistance to injury

KW - Signal transduction

KW - Transcription factors

KW - Trimethyltin

KW - mutPS-1 mice

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Mice expressing human mutant presenilin-1 exhibit decreased activation of NF-κB p50 in hippocampal neurons after injury

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

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