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The progression of Alzheimer’s dementia is associated with neurovasculature impairment, which includes inflammation, microthromboses, and reduced cerebral blood flow. Here, we investigate the effects of β amyloid peptides on the function of platelets, the cells driving haemostasis. Amyloid peptide β1‐42 (Aβ1‐42), Aβ1‐40, and Aβ25‐35 were tested in static adhesion experiments, and it was found that platelets preferentially adhere to Aβ1‐42 compared to other Aβ peptides. In addition, significant platelet spreading was observed over Aβ1‐42, while Aβ1‐40, Aβ25‐35, and the scAβ1‐42 control did not seem to induce any platelet spreading, which suggested that only Aβ1‐42 activates platelet signalling in our experimental conditions. Aβ1‐42 also induced significant platelet adhesion and thrombus formation in whole blood under venous flow condition, while other Aβ peptides did not. The molecular mechanism of …