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) Aβ1–40 and the genetic variants A2T and A2V which display increasing pathogenicity as A2T
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Somavarapu, A. K., Shen, F., Teilum, K., Zhang, J., Mossin, S., Thulstrup, P. W., … Hemmingsen, L. (2017). The Pathogenic A2V Mutant Exhibits Distinct Aggregation Kinetics, Metal Site Structure, and Metal Exchange of the Cu2+–Aβ Complex. Chemistry - A European Journal, 23(55), 13591–13595. https://doi.org/10.1002/chem.201703440
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