Roles for Fas in Programmed Cell Death of Motoneurons

  • C. Raoul
  • G. Ugolini
  • A. Estevez
  • B. Pettmann
  • C. E. Henderson
Conference paper
Part of the Research and Perspectives in Neurosciences book series (NEUROSCIENCE)

Summary

Over the last few years the distinction between naturally occurring and abnormal neuronal cell death mechanisms has become less clear. Not only have stress-related pathways been implicated in developmental programmed cell death, but neuronal loss in human neuro-degenerative disease or stroke has been shown to use some of the same mechanisms as classical apoptosis. The Fas receptor is a “killer molecule” most studied in the immune system. We review here some of the findings concerning its roles in neurons, focussing on results from our laboratory and from others concerning spinal motoneurons. There is now evidence that Fas activation is involved in certain forms of neuronal death, and that this process can be tightly controlled. It is too early to determine the precise role of Fas in the nervous system, either during development or in pathological situations. However, the existence of novel signalling pathways upstream and downstream of Fas in neurons suggests that, if Fas activation does contribute to loss of neurons in human patients, Fas-related pathways may provide a promising new set of targets for therapeutical intervention.

Keywords

Toxicity Ischemia Tyrosine Superoxide Retina 

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Copyright information

© Springer-Verlag Berlin Heidelberg 2001

Authors and Affiliations

  • C. Raoul
  • G. Ugolini
  • A. Estevez
  • B. Pettmann
  • C. E. Henderson

There are no affiliations available

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