Abstract
Extracellular aggregation of the β-amyloid (Aβ) peptide into toxic multimers in the brain is a prominent event occurring in the pathogenesis of Alzheimer's disease (AD), and a large amount of Aβ in the blood is derived from platelets. Thus, we speculated that platelets may play an important role in the process of AD. We first investigated the changes in platelet Aβ secretion with age. Then, we injected platelets from aged amyloid precursor protein APP/PS1 mice into young C57 mice and assessed their memory capacity along with their brain and peripheral blood Aβ expression levels. The Aβ content in mouse platelets increased with age. Exogenously aged APP/PS1 platelets changed the permeability of the blood-brain barrier in vitro, accelerating Aβ deposition in the brain and increasing the Aβ content in peripheral blood, leading to learning and memory deficits in the recipient mice. Subsequently, aspirin was administered to mice as an inhibitor of platelet activation, which effectively alleviated these toxic processes. Finally, we chose an in vitro blood-brain barrier model to explore the possible cytotoxicity of these platelets.