TY  - JOUR
AU  - Schemmert, Sarah
AU  - Schartmann, Elena
AU  - Zafiu, Christian
AU  - Kass, Bettina
AU  - Hartwig, Sonja
AU  - Lehr, Stefan
AU  - Bannach, Oliver
AU  - Langen, Karl-Josef
AU  - Shah, Nadim Joni
AU  - Kutzsche, Janine
AU  - Willuweit, Antje
AU  - Willbold, Dieter
TI  - Aβ Oligomer Elimination Restores Cognition in Transgenic Alzheimer’s Mice with Full-blown Pathology
JO  - Molecular neurobiology
VL  - 56
IS  - 3
SN  - 0893-7648
CY  - Totowa, NJ
PB  - Humana Press
M1  - FZJ-2018-04653
SP  - 2211-2223
PY  - 2019
AB  - Oligomers of the amyloid-β (Aβ) protein are suspected to be responsible for the development and progression of Alzheimer’s disease. Thus, the development of compounds that are able to eliminate already formed toxic Aβ oligomers is very desirable. Here, we describe the in vivo efficacy of the compound RD2, which was developed to directly and specifically eliminate toxic Aβ oligomers. In a truly therapeutic, rather than a preventive study, oral treatment with RD2 was able to reverse cognitive deficits and significantly reduce Aβ pathology in old-aged transgenic Alzheimer’s Disease mice with full-blown pathology and behavioral deficits. For the first time, we demonstrate the in vivo target engagement of RD2 by showing a significant reduction of Aβ oligomers in the brains of RD2-treated mice compared to placebo-treated mice. The correlation of Aβ elimination in vivo and the reversal of cognitive deficits in old-aged transgenic mice support the hypothesis that Aβ oligomers are relevant not only for disease development and progression, but also offer a promising target for the causal treatment of Alzheimer’s disease.
LB  - PUB:(DE-HGF)16
C6  - pmid:30003517
UR  - <Go to ISI:>//WOS:000460163700049
DO  - DOI:10.1007/s12035-018-1209-3
UR  - https://juser.fz-juelich.de/record/850919
ER  -