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Amyloid-beta peptide-receptor for advanced glycation endproduct interaction elicits neuronal expression of

S Du Yan1, H Zhu, J Fu

  • 1Department of Pathology, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.

Proceedings of the National Academy of Sciences of the United States of America
|May 13, 1997
PubMed

Insights

Alzheimer disease involves amyloid-beta activating neurons to release M-CSF, a factor that promotes microglial activation and contributes to AD pathogenesis. This M-CSF may serve as an early biomarker for neuronal issues in AD.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Neurons in Alzheimer disease (AD) are vulnerable to activated microglia.
  • Amyloid-beta peptide (Abeta) binding to neuronal receptors is a key factor in AD pathology.

Purpose of the Study:

  • To investigate the inflammatory pathway initiated by Abeta binding to neuronal RAGE.
  • To determine the role of M-CSF in Alzheimer disease pathogenesis and its potential as a biomarker.

Main Methods:

  • Examined Abeta-induced M-CSF production in neurons via an oxidant-sensitive, NF-kappaB-dependent pathway.
  • Analyzed M-CSF expression in AD brain tissue and cerebrospinal fluid (CSF).
  • Investigated M-CSF's effects on microglial activation, proliferation, and survival.

Main Results:

  • Abeta binding to neuronal RAGE induced M-CSF production.
  • Increased neuronal M-CSF expression was observed near Abeta deposits in AD brains.
  • CSF from AD patients showed a significant 5-fold increase in M-CSF levels compared to controls.
  • M-CSF stimulated microglial chemotaxis, proliferation, scavenger receptor and ApoE expression, and survival.

Conclusions:

  • Abeta-induced M-CSF release from neurons constitutes a novel inflammatory pathway in AD.
  • M-CSF contributes to AD pathogenesis by modulating microglial responses.
  • CSF M-CSF levels may indicate early neuronal perturbation in Alzheimer disease.

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