Apoptosis After Experimental Stroke: Fact or Fashion?

J Neurotrauma. 2000 Oct;17(10):899-914. doi: 10.1089/neu.2000.17.899.


This review examines the appearance of hallmarks of apoptosis following experimental stroke. The reviewed literature leaves no doubt that ischemic cell death in the brain is active, that is, requires energy; is gene directed, that is, requires new gene expression; and is capase-mediated, that is, uses apoptotic proteolytic machinery. However, sufficient differences to both classical necrosis and apoptosis exist which prevent easy mechanistic classification. It is concluded that ischemic cell death in the brain is neither necrosis nor apoptosis but is a chimera which appears on a continuum that has apoptosis and necrosis at the poles. The position on this continuum could be modulated by the intensity of the ischemic injury, the consequent availability of ATP and new protein synthesis, and both the age and context of the neuron in question. Thus the ischemic neuron may look necrotic but have actively died in an energy dependent manner with new gene expression and destruction via the apoptotic proteolytic machinery.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Brain Ischemia / genetics*
  • Brain Ischemia / metabolism
  • Brain Ischemia / physiopathology
  • Caspases / metabolism
  • Cell Nucleus / metabolism
  • Cell Nucleus / pathology
  • DNA Fragmentation / physiology
  • Disease Models, Animal
  • Gene Expression Regulation / physiology
  • Humans
  • Mitochondria / metabolism
  • Necrosis
  • Stroke / genetics*
  • Stroke / metabolism
  • Stroke / physiopathology


  • Caspases