β-Amyloid Protein Induces Platelet Aggregation and Supports Platelet Adhesion
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TL;DR
It is found that human beta AP peptide (1-40) fibrils aggregate platelets and support their adhesion, and these interactions are mediated through platelet membrane integrin receptors.
Abstract
The amyloid precursor protein (APP) is found in many cells including neurons, endothelial cells and blood platelets. Beta-amyloid protein (beta AP) is derived from APP and is deposited in brain and in cerebral microvasculature of individuals with Alzheimer's disease. In this study we demonstrate that beta AP interacts with human blood platelets. We found that human beta AP peptide (1-40) fibrils aggregate platelets and support their adhesion, and these interactions are mediated through platelet membrane integrin receptors.