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@INPROCEEDINGS{Fischer:283067,
author = {Fischer, Larissa and Adams, Jenna N and Molloy, Eóin N.
and Tremblay-Mercier, Jennifer and Remz, Jordana and
Binette, Alexa Pichet and Rajah, Natasha and Villeneuve,
Sylvia and Maass, Anne},
collaboration = {Group, PREVENT-AD Research},
title = {{C}hange in functional connectivity strength during rest
and encoding is differentially related to {A}lzheimer's
pathology and memory depending on {APOE} genotype},
journal = {Alzheimer's and dementia},
volume = {21},
number = {Suppl 2},
issn = {1552-5260},
reportid = {DZNE-2025-01474},
pages = {e100192},
year = {2025},
abstract = {The medial temporal lobe (MTL) and posteromedial cortex
(PMC) are essential for episodic memory and affected early
by Alzheimer's pathology, particularly in APOE4 carriers.
Functional connectivity (FC) changes within and between MTL
and PMC could be detrimental or beneficial for cognition.
However, the relation of those changes to Alzheimer's
pathology and memory performance is unclear and most studies
assess FC only during rest. We hypothesized that increasing
FC strength would be associated with higher pathology
burden, especially in APOE4 carriers.In this preregistered
study, we analysed longitudinal 3-Tesla fMRI over up to 4
years and cross-sectional amyloid-beta and tau PET
(PREVENT-AD cohort; details in Figure 1). We assessed
changes in resting-state FC (RSFC) and task-FC during
intentional object-location encoding within (ΔFCPMC,
ΔFCMTL) and between MTL and PMC (ΔFCMTL-PMC). The sample
included 152 cognitively unimpaired older adults
(63±5years, 102 female, 59 APOE4). We investigated
associations between ΔFC strength with i) pathology burden
and ii) change in delayed memory (RBANS composite score and
fMRI-task object recognition), and interactions with APOE
genotype. We used multiple regression and linear mixed
models including APOE, age, sex and education.We found ΔFC
by APOE interactions predicting pathology. Specifically,
declining RSFCPMC (p = 0.038; Figure 2a) was related to more
global amyloid in APOE4 carriers only. In contrast,
increasing encoding-FCMTL was related to more entorhinal tau
in APOE4 carriers only (p = 0.032, Figure 2b). Regarding
cognition, regardless of APOE status, increasing
encoding-FCPMC was related to decreasing RBANS (p = 0.018)
performance and object recognition (p = 0.001). Finally,
increasing RSFCMTL-PMC was related to increasing RBANS
performance (p = 0.032; Figure 3a), but increasing
encoding-FCMTL-PMC was related to decreasing object
recognition (p = 0.014; Figure 3b).Our study shows
APOE-dependent and region-specific associations of ΔFC
strength within and between episodic memory areas with
pathology burden and memory performance. Notably,
associations differed between RSFC and task-FC. In APOE4
carriers, longitudinally increasing FC or
'hyperconnectivity' within MTL during encoding was related
to tau in line with our hypothesis. However, in PMC,
longitudinally decreasing FC during rest was related to more
amyloid, indicating a disconnection in PMC regions. Our
study highlights that pathology-related network changes
manifest differentially during rest and task (memory
encoding).},
month = {Jul},
date = {2025-07-27},
organization = {Alzheimer’s Association
International Conference, Toronto
(Canada), 27 Jul 2025 - 31 Jul 2025},
keywords = {Humans / Female / Male / Magnetic Resonance Imaging /
Middle Aged / Biomarkers: metabolism / Apolipoprotein E4:
genetics / Aged / tau Proteins: metabolism /
Positron-Emission Tomography / Cross-Sectional Studies /
Alzheimer Disease: genetics / Alzheimer Disease: diagnostic
imaging / Alzheimer Disease: pathology / Amyloid
beta-Peptides: metabolism / Temporal Lobe: diagnostic
imaging / Temporal Lobe: pathology / Temporal Lobe:
metabolism / Longitudinal Studies / Neuropsychological Tests
/ Biomarkers (NLM Chemicals) / Apolipoprotein E4 (NLM
Chemicals) / tau Proteins (NLM Chemicals) / Amyloid
beta-Peptides (NLM Chemicals)},
cin = {AG Maaß},
ddc = {610},
cid = {I:(DE-2719)1311001},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
pubmed = {pmid:41447082},
pmc = {pmc:PMC12739621},
doi = {10.1002/alz70856_100192},
url = {https://pub.dzne.de/record/283067},
}