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@ARTICLE{Blmeke:1025964,
author = {Blömeke, Lara and Rehn, Fabian and Kraemer-Schulien,
Victoria and Kutzsche, Janine and Pils, Marlene and
Bujnicki, Tuyen and Lewczuk, Piotr and Kornhuber, Johannes
and Freiesleben, Silka D. and Schneider, Luisa-Sophie and
Preis, Lukas and Priller, Josef and Spruth, Eike J. and
Altenstein, Slawek and Lohse, Andrea and Schneider, Anja and
Fliessbach, Klaus and Wiltfang, Jens and Hansen, Niels and
Rostamzadeh, Ayda and Düzel, Emrah and Glanz, Wenzel and
Incesoy, Enise I. and Butryn, Michaela and Buerger,
Katharina and Janowitz, Daniel and Ewers, Michael and
Perneczky, Robert and Rauchmann, Boris-Stephan and Teipel,
Stefan and Kilimann, Ingo and Goerss, Doreen and Laske,
Christoph and Munk, Matthias H. and Sanzenbacher, Carolin
and Spottke, Annika and Roy-Kluth, Nina and Heneka, Michael
T. and Brosseron, Frederic and Wagner, Michael and
Wolfsgruber, Steffen and Kleineidam, Luca and Stark, Melina
and Schmid, Matthias and Jessen, Frank and Bannach, Oliver
and Willbold, Dieter and Peters, Oliver},
title = {{A}β oligomers peak in early stages of {A}lzheimer's
disease preceding tau pathology},
journal = {Alzheimer's $\&$ dementia / Diagnosis, assessment $\&$
disease monitoring},
volume = {16},
number = {2},
issn = {2352-8729},
address = {Hoboken, NJ},
publisher = {Wiley},
reportid = {FZJ-2024-03242},
pages = {e12589},
year = {2024},
abstract = {INTRODUCTION: Soluble amyloid beta (Aβ) oligomers have
been suggested as initiating Aβ related neuropathologic
change in Alzheimer’s disease (AD) but their quantitative
distribution and chronological sequence within the AD
continuum remain unclear.METHODS: A total of 526
participants in early clinical stages of AD and controls
from a longitudinal cohort were neurobiologically classified
for amyloid and tau pathology applying the AT(N) system. Aβ
and tau oligomers in the quantified cerebrospinal fluid
(CSF) were measured using surface-based fluorescence
intensity distribution analysis (sFIDA) technology.RESULTS:
Across groups, highest Aβ oligomer levels were found in A+
with subjective cognitive decline and mild cognitive
impairment.Aβ oligomers were significantly higher in A+T−
compared to A−T− and A+T+. APOE ε4 allele carriers
showed significantly higher Aβ oligomer levels. No
differences in tau oligomers were detected.DISCUSSION: The
accumulation of Aβ oligomers in the CSF peaks early within
the AD continuum, preceding tau pathology. Disease-modifying
treatments targeting Aβ oligomers might have the highest
therapeutic effect in these disease stages.},
cin = {IBI-7},
ddc = {610},
cid = {I:(DE-Juel1)IBI-7-20200312},
pnm = {5244 - Information Processing in Neuronal Networks
(POF4-524)},
pid = {G:(DE-HGF)POF4-5244},
typ = {PUB:(DE-HGF)16},
pubmed = {38666085},
UT = {WOS:001207849500001},
doi = {10.1002/dad2.12589},
url = {https://juser.fz-juelich.de/record/1025964},
}