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Original Contribution
April 1998

Platelet Activation in Alzheimer Disease

Author Affiliations

From the Departments of Psychiatry and Neurology (Dr Sevush) and the William J. Harrington Sr Center for Blood Diseases, Department of Medicine (Drs Jy, Kolodny, and Ahn, and Messrs Horstman and Mao), University of Miami School of Medicine, Miami, Fla.

Arch Neurol. 1998;55(4):530-536. doi:10.1001/archneur.55.4.530
Abstract

Background  In light of recent reports of diminished platelet serotonin concentration and increased plasma serotonin levels in patients with Alzheimer disease (AD), we hypothesized that a state of heightened platelet activation might be present in AD.

Objective  To compare baseline activation of unstimulated platelets in patients with AD with that in control subjects.

Patients and Methods  Flow cytometry was used to measure platelet activation in 91 patients with probable AD and 40 age-matched control subjects. Groups were compared for percentage of circulating platelet aggregates, expression of CD62p, formation of leukocyte-platelet complexes, and presence of circulating platelet microparticles, controlling for effects of demographic, clinical, physiological, and logistical factors.

Results  Multiple analysis of covariance on ranked data revealed a 39.5% increase in percentage of platelet aggregates (P=.0001), a 59.3% increase in expression of CD62p (P=.001), and a 53.3% increase in leukocyte-platelet complexes (P=.0001) in the group with AD but no differences in the number of platelet microparticles, overall platelet count, plasma fibrinogen level, or plasma platelet factor 3. Activation was weakly correlated with sex, but was independent of age, severity of disease, duration of disease, depression, agitation, and family history of dementia.

Conclusions  Platelets of patients with AD exhibit greater unstimulated activation than those of controls. Potential causes of such activation include possible stimulation of platelets by damaged cerebral endothelial cells or platelet activation induced by membrane abnormalities previously reported to be present in platelets of patients with AD. In light of recent evidence that platelets are the principal source of both amyloid precursor protein and β-amyloid peptide in human blood, it is possible that AD platelet activation may reflect or even contribute to the pathogenesis of the disease.

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