[Neuronal DNA damage correlates with a positive detection of c-Jun, nuclear factor kB, p53 and Par-4 transcription factors in Alzheimer's disease]

Rev Neurol. 2003 Jun;36(11):1004-10.
[Article in Spanish]

Abstract

Introduction and objectives: Alzheimer s disease is a neurodegenerative disorder characterized neuropathologically by beta amyloid plaques, neurofibrillary tangles, gliosis and neuronal loss. Recently, we have elucidated a molecular cascade of cell death induced by A beta 25 35 involving the activation of nuclear factor kappa B (NF kB), p53, and c Jun transcription factors in vitro. At present, no comparative reports have been published to establish a similar cell death signalization pathway in in vitro and in in vivo. The aim of this investigation was to determine if AD brains might activate NF kB, p53, c Jun, Par 4 transcription factors and to establish whether there exist a relationship between neuronal DNA damage and transcription factors activation.

Patients and methods: We investigated Ab plaques, neurofibrillary tangles and NF kB, p53, and c Jun transcription factor activation in five cerebral regions from 3 normal subjects and from six demented patient with sporadic AD and one patient with AD familiar according to CERAD criteria. Using TUNEL we determine neuronal damage.

Results: We demonstrated neuronal damage in 17 out of 50 regions evaluated as TUNEL positive, and their distribution was heterogeneous in all brain regions evaluated; and the activation of NF kB, p53, c Jun and Par 4 transcription factors from case # 24 and #22, corresponding to TUNEL positive.

Conclusions: We found a correlation between severity of DNA damage and nuclear activation of the transcription factors. These findings suggest that the AD brain may induce cell death by a molecular signalization similar to a non neuronal model by Ab exposure. This in situ study might validate previous Ab induced cell death observations in vitro.

Publication types

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

MeSH terms

  • Adult
  • Aged
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / analysis
  • Apoptosis / physiology
  • Apoptosis Regulatory Proteins
  • Carrier Proteins / analysis*
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • DNA Damage*
  • Female
  • Humans
  • In Situ Nick-End Labeling
  • Intracellular Signaling Peptides and Proteins*
  • Male
  • Middle Aged
  • NF-kappa B / analysis*
  • Neurons / chemistry*
  • Proto-Oncogene Proteins c-jun / analysis*
  • Statistics as Topic
  • Tumor Suppressor Protein p53 / analysis*

Substances

  • Amyloid beta-Peptides
  • Apoptosis Regulatory Proteins
  • Carrier Proteins
  • Intracellular Signaling Peptides and Proteins
  • NF-kappa B
  • Proto-Oncogene Proteins c-jun
  • Tumor Suppressor Protein p53
  • prostate apoptosis response-4 protein