Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Original Research Article
  • Published:

β-Amyloid augments platelet aggregation: reduced activity of familial angiopathy-associated mutants


The β-amyloid (Aβ) peptide is present both in serum and in platelets, however it is unclear whether Aβ plays a role in platelet function. We have now investigated the effects of soluble Aβ on platelet function and have found that low levels (0.1–1 nM) of soluble Aβ augment ADP-dependent platelet aggregation and translocation of focal adhesion kinase to the platelet cytoskeleton. Addition of Aβ to gel-filtered platelets along with concentrations of adenosine diphosphate (ADP) producing submaximal aggregation responses increased the aggregation response by over 2-fold depending on the ADP:Aβ ratios. The structure activity requirements for Aβ activity showed intriguing constraints. Only full length Aβ has significant activity. Truncated Aβ peptides, such as Aβ1–16 or Aβ25–35, or reverse Aβ40–1 all show little or no activity. We also examined the activity of mutant Aβ peptides, corresponding with the APP692A→G and APP693E→Q (at Aβ21 and Aβ22, respectively) which are found in familial Alzheimer's disease and hereditary cerebral hemorrhagic amyloidosis, Dutch type (HCHWA-D), and found that these peptides showed little or no activity. These results suggest that Aβ interacts with platelets in a highly specific manner and may play a role in regulating platelet function.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Similar content being viewed by others

Author information

Authors and Affiliations


Corresponding author

Correspondence to B Wolozin.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Wolozin, B., Maheshwari, S., Jones, C. et al. β-Amyloid augments platelet aggregation: reduced activity of familial angiopathy-associated mutants. Mol Psychiatry 3, 500–507 (1998).

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI:



Quick links