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Interleukin-6, beta-amyloid peptide and NMDA interactions in rat cortical neurons

Academic Article
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Overview

authors

  • Qiu, Z. H.
  • Gruol, Donna

publication date

  • June 2003

journal

  • Journal of Neuroimmunology  Journal

abstract

  • Neuronal damage in Alzheimer's disease (AD) is thought to involve direct toxicity of beta-amyloid peptide (Abeta) and excitotoxicity involving NMDA receptors (NMDARs) and altered Ca(2+) dynamics. Inflammation agents produced by microglia or astrocytes and associated with senile plaques such as the cytokine interleukin-6 (IL-6) could also contribute. To investigate this possibility, neuronal damage (lactate dehydrogenase assay, LDH, assay) was measured in cultures of rodent cortical neurons chronically treated with IL-6, Abeta or Abeta plus IL-6 and acutely treated with NMDA. Both Abeta and NMDA produced neuronal damage and this effect was larger with combined treatment. IL-6 did not produce significant neuronal damage but the largest neuronal damage was observed in cultures exposed to all three factors. IL-6 and Abeta enhanced Ca(2+) responses to NMDA and combined treatment produced the largest effect. These results are consistent with a role for interactions between Abeta, NMDA and IL-6 in the neuronal loss in AD.

subject areas

  • Alzheimer Disease
  • Amyloid beta-Peptides
  • Animals
  • Calcium Signaling
  • Cell Death
  • Cells, Cultured
  • Cerebral Cortex
  • Disease Models, Animal
  • Drug Interactions
  • Encephalitis
  • Excitatory Amino Acid Agonists
  • Fetus
  • Glutamic Acid
  • Interleukin-6
  • N-Methylaspartate
  • Nerve Degeneration
  • Neurons
  • Neurotoxins
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, N-Methyl-D-Aspartate
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Research

keywords

  • Alzheimer's disease
  • cytokine
  • excitotoxicity
  • intracellular Ca2+
  • neurotransmitter
  • senile plaques
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Identity

International Standard Serial Number (ISSN)

  • 0165-5728

Digital Object Identifier (DOI)

  • 10.1016/s0165-5728(03)00158-9

PubMed ID

  • 12799020
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Additional Document Info

start page

  • 51

end page

  • 57

volume

  • 139

issue

  • 1-2

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