Amyloid beta-protein: experiment and theory on the 21-30 fragment

J Phys Chem B. 2009 Apr 30;113(17):6041-6. doi: 10.1021/jp808384x.

Abstract

The structure of the 21-30 fragment of the amyloid beta-protein (Abeta) was investigated by ion mobility mass spectrometry and replica exchange dynamics simulations. Mutations associated with familial Alzheimer's disease (E22G, E22Q, E22K, and D23N) of Abeta(21-30) were also studied, in order to understand any structural changes that might occur with these substitutions. The structure of the WT peptide shows a bend and a perpendicular turn in the backbone which is maintained by a network of D23 hydrogen bonding. Results for the mutants show that substitutions at E22 do little to alter the overall structure of the fragment. A substitution at D23 resulted in a change of structure for Abeta(21-30). A comparison of these gas-phase studies to previous solution-phase studies reveals that the peptide can fold in the absence of solvent to a structure also seen in solution, highlighting the important role of the D23 hydrogen bonding network in stabilizing the fragment's folded structure.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Amyloid beta-Peptides / chemistry*
  • Amyloid beta-Peptides / genetics
  • Computer Simulation
  • Gases / chemistry
  • Hydrogen Bonding
  • Models, Chemical
  • Models, Molecular
  • Mutation
  • Peptide Fragments / chemistry*
  • Peptide Fragments / genetics
  • Solutions
  • Spectrometry, Mass, Electrospray Ionization

Substances

  • Amyloid beta-Peptides
  • Gases
  • Peptide Fragments
  • Solutions
  • amyloid beta-protein (21-30)