Title

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

Document Type

Journal Article

Publisher

Taylor & Francis Group

School

Centre of Excellence for Alzheimer's Disease Research and Care / School of Medical Sciences

RAS ID

25875

Comments

Originally published as:

Elaskalani, O., Khan, I., Morici, M., Matthysen, C., Sabale, M., Martins, R. N., ... & Metharom, P. (2017). Oligomeric and fibrillar amyloid beta 42 induce platelet aggregation partially through GPVI. Platelets. Advance online publication. doi:10.1080/09537104.2017.1401057

Original article available here.

Abstract

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.

DOI

10.1080/09537104.2017.1401057

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