The Pathogenic A2V Mutant Exhibits Distinct Aggregation Kinetics, Metal Site Structure, and Metal Exchange of the Cu2+-A[beta] 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) A[beta]1-40 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
Hauptverfasser: Somavarapu, Arun K, Shen, Fei, Teilum, Kaare, Zhang, Jingdong, Mossin, Susanne, Thulstrup, Peter W, Bjerrum, Morten J, Tiwari, Manish K, Szunyogh, Daniel, Sotofte, Peter M, Kepp, Kasper P, Hemmingsen, Lars
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Sprache:eng
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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) A[beta]1-40 and the genetic variants A2T and A2V which display increasing pathogenicity as A2T
ISSN:0947-6539
1521-3765
DOI:10.1002/chem.201703440