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Apoptosis and brain ischaemia.

Seth Love1

  • 1Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, BS16 1LE, Bristol, UK. seth.love@bris.ac.uk

Progress in Neuro-Psychopharmacology & Biological Psychiatry
|March 27, 2003
PubMed
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Brain ischemia triggers neuronal death via caspases, key apoptosis proteases. This process involves mitochondrial pathways and transcription factors, offering potential therapeutic targets for stroke interventions.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Neuronal death following brain ischemia is increasingly linked to caspases, proteases central to apoptosis.
  • This caspase-mediated death, while not always morphologically apoptotic, is more pronounced in transient focal ischemia and contributes to delayed neuronal loss in infarct penumbras.

Purpose of the Study:

  • To elucidate the mechanisms of caspase activation and neuronal death after brain ischemia.
  • To identify potential therapeutic targets for mitigating ischemic brain damage.

Main Methods:

  • The study reviews evidence on caspase activation pathways, including mitochondrial outer membrane permeabilization and the role of Bcl-2 family proteins.
  • It examines the involvement of various transcription factors (NF-kappaB, c-Jun, p53, E2F1) and signaling molecules (Akt, Smac/DIABLO).

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Main Results:

  • Caspase activation is initiated by the translocation of pro-apoptotic proteins (Bax, Bak, BH3-only) to mitochondria, releasing cytochrome c, procaspase-9, and Apaf-1.
  • Regulation involves transcription factors, Akt inactivation, Smac/DIABLO release, lipid peroxidation, reduced protein synthesis, and cell cycle reentry.
  • Non-caspase apoptosis appears to play a minor role in ischemic brain damage.

Conclusions:

  • Caspase-mediated neuronal death is a significant contributor to brain damage after ischemia.
  • The intracellular pathways involved present potential therapeutic targets.
  • Anti-apoptotic strategies require careful evaluation to ensure preservation of neuronal function, not just survival.