TY  - JOUR
AU  - Blömeke, Lara
AU  - Rehn, Fabian
AU  - Kraemer-Schulien, Victoria
AU  - Kutzsche, Janine
AU  - Pils, Marlene
AU  - Bujnicki, Tuyen
AU  - Lewczuk, Piotr
AU  - Kornhuber, Johannes
AU  - Freiesleben, Silka D.
AU  - Schneider, Luisa-Sophie
AU  - Preis, Lukas
AU  - Priller, Josef
AU  - Spruth, Eike J.
AU  - Altenstein, Slawek
AU  - Lohse, Andrea
AU  - Schneider, Anja
AU  - Fliessbach, Klaus
AU  - Wiltfang, Jens
AU  - Hansen, Niels
AU  - Rostamzadeh, Ayda
AU  - Düzel, Emrah
AU  - Glanz, Wenzel
AU  - Incesoy, Enise I.
AU  - Butryn, Michaela
AU  - Buerger, Katharina
AU  - Janowitz, Daniel
AU  - Ewers, Michael
AU  - Perneczky, Robert
AU  - Rauchmann, Boris-Stephan
AU  - Teipel, Stefan
AU  - Kilimann, Ingo
AU  - Goerss, Doreen
AU  - Laske, Christoph
AU  - Munk, Matthias H.
AU  - Sanzenbacher, Carolin
AU  - Spottke, Annika
AU  - Roy-Kluth, Nina
AU  - Heneka, Michael T.
AU  - Brosseron, Frederic
AU  - Wagner, Michael
AU  - Wolfsgruber, Steffen
AU  - Kleineidam, Luca
AU  - Stark, Melina
AU  - Schmid, Matthias
AU  - Jessen, Frank
AU  - Bannach, Oliver
AU  - Willbold, Dieter
AU  - Peters, Oliver
TI  - Aβ oligomers peak in early stages of Alzheimer's disease preceding tau pathology
JO  - Alzheimer's & dementia / Diagnosis, assessment & disease monitoring
VL  - 16
IS  - 2
SN  - 2352-8729
CY  - Hoboken, NJ
PB  - Wiley
M1  - FZJ-2024-03242
SP  - e12589
PY  - 2024
AB  - 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.
LB  - PUB:(DE-HGF)16
C6  - 38666085
UR  - <Go to ISI:>//WOS:001207849500001
DO  - DOI:10.1002/dad2.12589
UR  - https://juser.fz-juelich.de/record/1025964
ER  -