The Pathogenic A2V Mutant Exhibits Distinct Aggregation Kinetics, Metal Site Structure, and Metal Exchange of the Cu2+–Aβ Complex

The Pathogenic A2V Mutant Exhibits Distinct Aggregation Kinetics, Metal Site Structure, and Metal Exchange of the Cu2+–Aβ Complex

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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Veröffentlicht in:Chemistry : a European journal 2017-10, Vol.23 (55), p.13591-13595
Hauptverfasser: Somavarapu, Arun K., Shen, Fei, Teilum, Kaare, Zhang, Jingdong, Mossin, Susanne, Thulstrup, Peter W., Bjerrum, Morten J., Tiwari, Manish K., Szunyogh, Daniel, Søtofte, Peter M., Kepp, Kasper P., Hemmingsen, Lars
Format: Artikel
Sprache:eng
Schlagworte:
Alzheimer's disease
amyloid beta
copper
kinetics
oligomers
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Zusammenfassung: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
ISSN:0947-6539
1521-3765
DOI:10.1002/chem.201703440