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Pathological immuno-reactions of glial cells in Alzheimer’s disease and possible sites of interference

  • P. Schubert
  • T. Ogata
  • H. Miyazaki
  • C. Marchini
  • S. Ferroni
  • K. Rudolphi
Part of the Journal of Neural Transmission. Supplementa book series (NEURAL SUPPL, volume 54)

Summary

A significant role of a pathological glial cell activation in the pathogenesis of Alzheimer’s disease is supported by the growing evidence that inflammatory proteins, which are produced by reactive astrocytes, promote the transformation of diffuse β-amyloid deposits into the filamentous, neurotoxic form. A number of vicious circles, driven by the release of TNF-a and free oxygen radicals from microglial cells, may cause an upregulated microglial activation and their production of interleukin-1 which triggers, secondarily, the crucial activation of astrocytes. Reactive functional changes of glial cells seem to be controlled by an altered balance of the second messengers Ca2+ and cAMP and can be counterregulated by the endogenous cell modulator adenosine which strenghtens the cAMP-dependent signalling chain. A further reinforcement of the homeostatic adenosine effects on glial cells by pharmaca, such as propentofylline, may add to neuroprotection in Alzheimer’s disease.

Keywords

Glial Cell Microglial Cell Inflammatory Protein cAMP Signalling Cereb Blood Flow 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag/Wien 1998

Authors and Affiliations

  • P. Schubert
    • 1
  • T. Ogata
    • 1
  • H. Miyazaki
    • 1
  • C. Marchini
    • 1
    • 2
  • S. Ferroni
    • 2
  • K. Rudolphi
    • 3
  1. 1.Department of NeuromorphologyMax Planck Institute for NeurobiologyMartinsriedFederal Republic of Germany
  2. 2.Hoechst Marion RousselFrankfurtFederal Republic of Germany
  3. 3.Department of PhysiologyUniversity of BolognaItaly

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