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 | |
| 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.).
Funding
This research was supported by NIH Grant RO1 NS39141-01A2 and American Heart Association Grants 9930072N (K.R.P.) and 0120233B (T.L.B.).
| Funders | Funder number |
|---|---|
| National Institutes of Health (NIH) | RO1 NS39141-01A2 |
| National Institute of Neurological Disorders and Stroke | R01NS039141 |
| American Heart Association | 0120233B, 9930072N |
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
