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

作者: S Nagula , N R Shulman , T Sunderland , A Bush , B Wolozin

DOI: 10.1038/SJ.MP.4000451

关键词:

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

参考文章(0)