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@ARTICLE{Wallin:823867,
author = {Wallin, C. and Kulkarni, Y. S. and Abelein, A and Jarvet,
J. and Liao, Qinghua and Strodel, Birgit and Olsson, L. and
Luo, J. and Abrahams, J. P. and Sholts, S. B. and Roos, P.
M. and Kamerlin, S. C. L. and Gräslund, A. and
Wärmländer, S. K. T. S.},
title = {{C}haracterization of {M}n({II}) ion binding to the
amyloid-ß peptide in {A}lzheimer’s disease},
journal = {Journal of trace elements in medicine and biology},
volume = {38},
issn = {0946-672X},
address = {München},
publisher = {Elsevier},
reportid = {FZJ-2016-06507},
pages = {183-193},
year = {2016},
abstract = {Growing evidence links neurodegenerative diseases to metal
exposure. Aberrant metal ion concentrationshave been noted
in Alzheimer’s disease (AD) brains, yet the role of metals
in AD pathogenesis remainsunresolved. A major factor in AD
pathogenesis is considered to be aggregation of and amyloid
formationby amyloid-ß (Aß) peptides. Previous studies have
shown that Aß displays specific binding to Cu(II)and Zn(II)
ions, and such binding has been shown to modulate Aß
aggregation. Here, we use nuclearmagnetic resonance (NMR)
spectroscopy to show that Mn(II) ions also bind to the
N-terminal part ofthe Aß(1–40) peptide, with a weak
binding affinity in the milli- to micromolar range. Circular
dichroism(CD) spectroscopy, solid state atomic force
microscopy (AFM), fluorescence spectroscopy, and
molecularmodeling suggest that the weak binding of Mn(II) to
Aß may not have a large effect on the
peptide’saggregation into amyloid fibrils. However,
identification of an additional metal ion displaying Aß
bindingreveals more complex AD metal chemistry than has been
previously considered in the literature.},
cin = {ICS-6},
ddc = {570},
cid = {I:(DE-Juel1)ICS-6-20110106},
pnm = {553 - Physical Basis of Diseases (POF3-553)},
pid = {G:(DE-HGF)POF3-553},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000385473600023},
pubmed = {pmid:27085215},
doi = {10.1016/j.jtemb.2016.03.009},
url = {https://juser.fz-juelich.de/record/823867},
}