Abstract
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 language | English |
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Pages (from-to) | 509-513 |
Number of pages | 5 |
Journal | NeuroReport |
Volume | 15 |
Issue number | 3 |
DOIs | |
Publication status | Published - Mar 2004 |
Keywords
- Amyloid-β
- Neurotoxicity
- Phospholipase A
- Platelet activating factor
- Prions
- Prostaglandins
ASJC Scopus subject areas
- Neuroscience(all)