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

Dement Geriatr Cogn Disord. 2003;16(2):93-7. doi: 10.1159/000070681.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease
  • Amyloid Precursor Protein Secretases
  • Amyloid beta-Peptides / blood*
  • Aspartic Acid Endopeptidases / blood
  • Blood Platelets / metabolism*
  • Endopeptidases
  • Humans
  • Membrane Proteins / blood
  • Peptide Fragments / blood*
  • Platelet Activation
  • Presenilin-1

Substances

  • Amyloid beta-Peptides
  • Membrane Proteins
  • PSEN1 protein, human
  • Peptide Fragments
  • Presenilin-1
  • amyloid beta-protein (1-40)
  • amyloid beta-protein (1-42)
  • Amyloid Precursor Protein Secretases
  • Endopeptidases
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human