Related Experiment Video
Updated: Aug 24, 2026

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans
Published on: January 8, 2015
The role of platelet activating factor in prion and amyloid-beta neurotoxicity
Clive Bate1, Mario Salmona, Alun Williams
1Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, UK. c.bate@vet.gla.ac.uk
Abstract:
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.
Related Concept Videos
Amyloid Fibrils
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Alzheimer Disease ll: Pathophysiology
Parkinson Disease ll: Pathophysiology
Alzheimer Disease l: Introduction

