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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

Producción científica: Articlerevisión exhaustiva

24 Citas (Scopus)

Resumen

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.

Idioma originalEnglish
Páginas (desde-hasta)152-157
Número de páginas6
PublicaciónMolecular Brain Research
Volumen110
N.º1
DOI
EstadoPublished - ene 31 2003

Nota bibliográfica

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.).

Financiación

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

FinanciadoresNúmero del financiador
National Institutes of Health (NIH)RO1 NS39141-01A2
National Institute of Neurological Disorders and StrokeR01NS039141
American Heart Association0120233B, 9930072N

    ODS de las Naciones Unidas

    Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible

    1. Good health and well being
      Good health and well being

    ASJC Scopus subject areas

    • Molecular Biology
    • Cellular and Molecular Neuroscience

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