ABSTRACT
A prominent current hypothesis is that impaired metal ion homeostasis may contribute to Alzheimer's disease (AD). We elucidate the interaction of Cu2+ with wild-type (WT) Aß1-40 and the genetic variants A2T and A2V which display increasing pathogenicity as A2TSubject(s)
Amyloid beta-Peptides/chemistry
, Copper/chemistry
, Alzheimer Disease/metabolism
, Alzheimer Disease/pathology
, Amyloid beta-Peptides/genetics
, Amyloid beta-Peptides/metabolism
, Circular Dichroism
, Electron Spin Resonance Spectroscopy
, Humans
, Kinetics
, Microscopy, Atomic Force
, Mutagenesis, Site-Directed
, Peptide Fragments/chemistry
, Peptide Fragments/genetics
, Peptide Fragments/metabolism