NR AQGU
AU Bate,C.; Salmona,M.; Williams,A.
TI The role of platelet activating factor in prion and amyloid-beta neurotoxicity
QU Neuroreport 2004 Mar 1; 15(3): 509-13
PT journal article
AB In the prion diseases, neurodegeneration is preceded by the accumulation of the disease-associated isoform of the prion protein (PrP). In the present study, neurones treated with three different phospholipase A2 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-beta1-42). Further studies showed that neurones pre-treated with platelet activating factor (PAF) antagonists were equally resistant to PrP peptides or amyloid-beta1-42. 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.
MH Amyloid beta-Protein/*toxicity; Brain Neoplasms; Caspases/metabolism; Cell Death; Dinoprostone/metabolism; Human; Nervous System Diseases/*chemically induced/*pathology; Neuroblastoma; Peptide Fragments/*toxicity; Phospholipases A/antagonists & inhibitors; Platelet Activating Factor/*physiology; Prions/*toxicity; Support, Non-U.S. Gov't; Tumor Cells, Cultured
AD Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, UK. c.bate@vet.gla.ac.uk
SP englisch
PO England