Platelet Activation in Alzheimer Disease

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Abstract
ALTHOUGH principally a disease of the brain, Alzheimer disease (AD) has also been associated with peripheral manifestations.1 Platelets have received particular attention in this regard, with reported abnormalities including increased membrane fluidity,2,3 increased α2-adrenoreceptor binding,4 increased monoamine oxidase activity,5,6 reduced cytochrome c oxidase activity,7 increased protein kinase C activity,8 and reduced phospholipase C activity.9 Platelets have also recently been shown to be the principal source of both amyloid precursor protein and β-amyloid peptide in human blood.10,11