Oligomeric and fibrillar amyloid beta 42 induce platelet aggregation partially through GPVI

O. Elaskalani, I. Khan, M. Morici, C. Matthysen, M. Sabale, R. N. Martins, G. Verdile, P. Metharom*

*Corresponding author for this work

Research output: Contribution to journalArticle

3 Citations (Scopus)


The effects of the Alzheimer’s disease (AD)-associated Amyloid-β (Aβ) peptides on platelet aggregation have been previously assessed, but most of these studies focused on Aβ40 species. It also remains to be determined which distinct forms of Aβ peptides exert differential effects on platelets. In AD, oligomeric Aβ42 species is widely thought to be a major contributor to the disease pathogenesis. We, therefore, examine the ability of oligomeric and fibrillary Aβ42 to affect platelet aggregation. We show that both forms of Aβ42 induced significant platelet aggregation and that it is a novel ligand for the platelet receptor GPVI. Furthermore, a novel binding peptide that reduces the formation of soluble Aβ42 oligomers was effective at preventing Aβ42-dependent platelet aggregation. These results support a role for Aβ42 oligomers in platelet hyperactivity.

Original languageEnglish
Pages (from-to)415-420
Number of pages6
Issue number4
Publication statusPublished - 19 May 2018



  • Amyloid beta
  • platelet aggregation

Cite this