TY - JOUR
AU - Kroth, H.
AU - Ansaloni, A.
AU - Varisco, Y.
AU - Jan, A.
AU - Sreenivasachary, N.
AU - Rezaei-Ghaleh, N.
AU - Giriens, V.
AU - Lohmann, S.
AU - Pilar López-Deber, M.
AU - Adolfsson, O.
AU - Pihlgren, M.
AU - Paganetti, P.
AU - Froestl, W.
AU - Nagel-Steger, L.
AU - Willbold, D
AU - Schrader, T
AU - Zweckstetter, M.
AU - Pfeifer, A.
AU - Lashuel, H.A.
AU - Muhs, A.
TI - Discovery and structure activity relationship of small molecule inhibitors of toxic-ß--amyloid-42 fibril formation
JO - The journal of biological chemistry
VL - 287
SN - 0021-9258
CY - Bethesda, Md.
PB - Soc.
M1 - PreJuSER-23050
SP - 34786 - 34800
PY - 2012
N1 - Record converted from VDB: 12.11.2012
AB - Increasing evidence implicates Aβ peptides self-assembly and fibril formation as crucial events in the pathogenesis of Alzheimer disease. Thus, inhibiting Aβ aggregation, among others, has emerged as a potential therapeutic intervention for this disorder. Herein, we employed 3-aminopyrazole as a key fragment in our design of non-dye compounds capable of interacting with Aβ42 via a donor-acceptor-donor hydrogen bond pattern complementary to that of the β-sheet conformation of Aβ42. The initial design of the compounds was based on connecting two 3-aminopyrazole moieties via a linker to identify suitable scaffold molecules. Additional aryl substitutions on the two 3-aminopyrazole moieties were also explored to enhance π-π stacking/hydrophobic interactions with amino acids of Aβ42. The efficacy of these compounds on inhibiting Aβ fibril formation and toxicity in vitro was assessed using a combination of biophysical techniques and viability assays. Using structure activity relationship data from the in vitro assays, we identified compounds capable of preventing pathological self-assembly of Aβ42 leading to decreased cell toxicity.
LB - PUB:(DE-HGF)16
C6 - pmid:22891248
C2 - pmc:PMC3464581
UR - <Go to ISI:>//WOS:000309654200078
DO - DOI:10.1074/jbc.M112.357665
UR - https://juser.fz-juelich.de/record/23050
ER -