Unaltered plasma levels of beta-amyloid(1-40) and beta-amyloid(1-42) upon stimulation of human platelets

Dementia and Geriatric Cognitive Disorders
Annika OlssonKaj Blennow

Abstract

Accumulation of beta-amyloid (Abeta) in the brain is one of the central lesions in Alzheimer's disease (AD). Alternative cleavage of the amyloid precursor protein (APP), occurring in both normal and AD subjects, results in the generation and secretion of soluble APP, Abeta(40) and Abeta(42). Platelets have been regarded as the primary source of circulating APP and Abeta. Plasma levels of Abeta may therefore be dependent on platelet activation. We analysed Abeta(40/42) in plasma in the presence of physiological agonists of platelet activation such as adenosine diphosphate, collagen, thrombin, and a synthetic agonist, thrombin receptor activator peptide 6. We found that the levels of Abeta(40/42) in plasma were not related to platelet activation, suggesting that sampling techniques affecting platelet activation do not confound measurement of Abeta(40/42 )in plasma.

Citations

Dec 25, 2007·Journal of Psychiatric Research·Imrich BlaskoPeter Fischer
Jan 13, 2009·Drug Discovery Today·Paul W Thompson, Andrew Lockhart
Apr 4, 2006·Neurochemical Research·Nunzio PomaraBruce G Pollock
Aug 31, 2006·Journal of Chromatography. B, Analytical Technologies in the Biomedical and Life Sciences·J Randall SlemmonPeter Seubert

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