Research ArticlePhysiology

Platelets contribute to amyloid-β aggregation in cerebral vessels through integrin αIIbβ3–induced outside-in signaling and clusterin release

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Science Signaling  24 May 2016:
Vol. 9, Issue 429, pp. ra52
DOI: 10.1126/scisignal.aaf6240

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Antiplatelet drugs for Alzheimer’s patients

Patients with Alzheimer’s disease (AD) often have pathological amyloid-β (Aβ) plaques in the brain parenchymal tissue and in cerebral blood vessels with adhesive or aggregated platelets. In the blood vessels, Aβ aggregates cause the vascular dysfunction disorder cerebral amyloid angiopathy (CAA), which contributes to AD progression. Donner et al. found that Aβ bound and stimulated the integrin αIIbβ3 on cultured human and mouse platelets, creating a feed-forward loop involving the secretion of clusterin and adenosine diphosphate, which in turn promoted Aβ aggregation and perpetuated platelet activation, respectively. Treatment with the platelet activation inhibitor clopidogrel decreased CAA burden in AD model mice, suggesting that antiplatelet therapy might ameliorate vascular symptoms contributing to dementia in AD patients.

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