Prevention of amyloid-β fibril formation using antibodies against the C-terminal region of amyloid-β1-40 and amyloid-β1-42

J Alzheimers Dis. 2013;34(1):133-7. doi: 10.3233/JAD-120850.

Abstract

Alzheimer's disease is characterized by the abnormal aggregation of amyloid-β (Aβ)1-40 and Aβ1-42 peptides into fibrils. In this work, we analyzed the kinetics of Aβ1-40 and Aβ1-42 fibril formation in vitro using Thioflavin T fluorescence. We synthesized high-purity peptides and performed a hexafluoro-2-propanol pre-treatment to yield uniform peptide solutions as starting materials. We found that the aggregation is clearly affected by the presence of sub-millimolar quantities of antibodies against the C-terminal region of the peptides. Because the fibrillization of these peptides is closely related to the pathogenesis of Alzheimer's disease, blocking this process may provide significant therapeutic benefit.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid / drug effects*
  • Amyloid / ultrastructure
  • Amyloid beta-Peptides / chemistry*
  • Amyloid beta-Peptides / immunology*
  • Amyloid beta-Peptides / pharmacology
  • Antibodies / pharmacology*
  • Dose-Response Relationship, Drug
  • Humans
  • In Vitro Techniques
  • Microscopy, Electron, Transmission
  • Peptide Fragments / chemistry*
  • Peptide Fragments / immunology*
  • Peptide Fragments / pharmacology
  • Propanols
  • Time Factors

Substances

  • Amyloid
  • Amyloid beta-Peptides
  • Antibodies
  • Peptide Fragments
  • Propanols
  • amyloid beta-protein (1-40)
  • amyloid beta-protein (1-42)
  • hexafluoroisopropanol