Post-ischemic brain damage: NF-kappaB dimer heterogeneity as a molecular determinant of neuron vulnerability

FEBS J. 2009 Jan;276(1):27-35. doi: 10.1111/j.1742-4658.2008.06767.x.


Nuclear factor-kappaB (NF-kappaB) has been proposed to serve a dual function as a regulator of neuron survival in pathological conditions associated with neurodegeneration. NF-kappaB is a transcription family of factors comprising five different proteins, namely p50, RelA/p65, c-Rel, RelB and p52, which can combine differently to form active dimers in response to external stimuli. Recent research shows that diverse NF-kappaB dimers lead to cell death or cell survival in neurons exposed to ischemic injury. While the p50/p65 dimer participates in the pathogenesis of post-ischemic injury by inducing pro-apoptotic gene expression, c-Rel-containing dimers increase neuron resistance to ischemia by inducing anti-apoptotic gene transcription. We present, in this report, the latest findings and consider the therapeutic potential of targeting different NF-kappaB dimers to limit ischemia-associated neurodegeneration.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Brain Damage, Chronic / etiology*
  • Brain Damage, Chronic / pathology
  • Brain Damage, Chronic / physiopathology
  • Brain Ischemia / pathology
  • Brain Ischemia / physiopathology*
  • Dimerization
  • Gene Expression Regulation
  • Humans
  • NF-kappa B / physiology*
  • Neurons / pathology*
  • Transcription Factors / metabolism


  • NF-kappa B
  • Transcription Factors