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Amyloid β-Protein: Experiment and Theory on the 21−30 Fragment
- Murray, Megan M;
- Krone, Mary Griffin;
- Bernstein, Summer L;
- Baumketner, Andrij;
- Condron, Margaret M;
- Lazo, Noel D;
- Teplow, David B;
- Wyttenbach, Thomas;
- Shea, Joan-Emma;
- Bowers, Michael T
Published Web Location
https://doi.org/10.1021/jp808384xAbstract
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.
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