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@ARTICLE{Cavini:856101,
author = {Cavini, Italo A. and Munte, Claudia E. and Erlach, Markus
Beck and van Groen, Thomas and Kadish, Inga and Zhang, Tao
and Ziehm, Tamar and Nagel-Steger, Luitgard and Kutzsche,
Janine and Kremer, Werner and Willbold, Dieter and
Kalbitzer, Hans Robert},
title = {{I}nhibition of amyloid {A}β aggregation by high pressures
or specific {D}-enantiomeric peptides},
journal = {Chemical communications},
volume = {54},
number = {26},
issn = {1364-548X},
address = {Cambridge},
publisher = {Soc.},
reportid = {FZJ-2018-05747},
pages = {3294 - 3297},
year = {2018},
abstract = {Pressure can shift the polymer–monomer equilibrium of
Aβ, increasing pressure first leads to a release of
Aβ-monomers, surprisingly at pressures higher than 180 MPa
repolymerization is induced. By high pressure NMR
spectroscopy, differences of partial molar volumes ΔV0 and
compressibility factors Δβ′ of polymerization were
determined at different temperatures. The D-enantiomeric
peptides RD2 and RD2D3 bind to monomeric Aβ with affinities
substantially higher than those determined for fibril
formation. By reducing the Aβ concentration below the
critical concentration for polymerization they inhibit the
formation of toxic oligomers. Chemical shift perturbation
allows the identification of the binding sites. The
D-peptides are candidates for drugs preventing Alzheimer's
disease. We show that RD2D3 has a positive effect on the
cognitive behaviour of transgenic (APPSwDI) mice prone to
Alzheimer's disease. The heterodimer complexes have a
smaller Stokes radius than Aβ alone indicating the
recognition of a more compact conformation of Aβ identified
by high pressure NMR before.},
cin = {ICS-6},
ddc = {540},
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},
pubmed = {pmid:29537428},
UT = {WOS:000428553500024},
doi = {10.1039/C8CC01458B},
url = {https://juser.fz-juelich.de/record/856101},
}