The role of platelet activating factor in prion and amyloid-β neurotoxicity

Clive Bate, Mario Salmona, Alun Williams

Research output: Contribution to journalArticlepeer-review


In the priori diseases, neurodegeneration is preceded by the accumulation of the disease-associated isoform of the prion protein (PrPd). In the present study, neurones treated with three different phospholipase A 2 inhibitors were resistant to the toxic effects of PrP peptides or a synthetic miniprion (sPrP106). Phospholipase A2 inhibitors also protected neurones against a toxic peptide found in Alzheimer's disease (amyloid-β1-42). Further studies showed that neurones pre-treated with platelet activating factor (PAF) antagonists were equally resistant to PrP peptides or amyloid-β1-42. Moreover, both phospholipase A2 inhibitors and PAF antagonists reduced the activation of caspase-3, a marker of apoptosis, and the production of prostaglandin E2 that is closely associated with neuronal death in prion or Alzheimer's diseases.

Original languageEnglish
Pages (from-to)509-513
Number of pages5
Issue number3
Publication statusPublished - Mar 2004


  • Amyloid-β
  • Neurotoxicity
  • Phospholipase A
  • Platelet activating factor
  • Prions
  • Prostaglandins

ASJC Scopus subject areas

  • Neuroscience(all)


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