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000283067 041__ $$aEnglish
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000283067 1001_ $$0P:(DE-2719)9002356$$aFischer, Larissa$$b0$$eFirst author
000283067 1112_ $$aAlzheimer’s Association International Conference$$cToronto$$d2025-07-27 - 2025-07-31$$gAAIC 25$$wCanada
000283067 245__ $$aChange in functional connectivity strength during rest and encoding is differentially related to Alzheimer's pathology and memory depending on APOE genotype
000283067 260__ $$c2025
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000283067 520__ $$aThe 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).
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000283067 650_7 $$2NLM Chemicals$$aBiomarkers
000283067 650_7 $$2NLM Chemicals$$aApolipoprotein E4
000283067 650_7 $$2NLM Chemicals$$atau Proteins
000283067 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000283067 650_2 $$2MeSH$$aHumans
000283067 650_2 $$2MeSH$$aFemale
000283067 650_2 $$2MeSH$$aMale
000283067 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000283067 650_2 $$2MeSH$$aMiddle Aged
000283067 650_2 $$2MeSH$$aBiomarkers: metabolism
000283067 650_2 $$2MeSH$$aApolipoprotein E4: genetics
000283067 650_2 $$2MeSH$$aAged
000283067 650_2 $$2MeSH$$atau Proteins: metabolism
000283067 650_2 $$2MeSH$$aPositron-Emission Tomography
000283067 650_2 $$2MeSH$$aCross-Sectional Studies
000283067 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000283067 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000283067 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000283067 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000283067 650_2 $$2MeSH$$aTemporal Lobe: diagnostic imaging
000283067 650_2 $$2MeSH$$aTemporal Lobe: pathology
000283067 650_2 $$2MeSH$$aTemporal Lobe: metabolism
000283067 650_2 $$2MeSH$$aLongitudinal Studies
000283067 650_2 $$2MeSH$$aNeuropsychological Tests
000283067 7001_ $$aAdams, Jenna N$$b1
000283067 7001_ $$0P:(DE-2719)9002180$$aMolloy, Eóin N.$$b2
000283067 7001_ $$aTremblay-Mercier, Jennifer$$b3
000283067 7001_ $$aRemz, Jordana$$b4
000283067 7001_ $$aBinette, Alexa Pichet$$b5
000283067 7001_ $$aRajah, Natasha$$b6
000283067 7001_ $$aVilleneuve, Sylvia$$b7
000283067 7001_ $$0P:(DE-2719)2811815$$aMaass, Anne$$b8$$eLast author
000283067 7001_ $$aGroup, PREVENT-AD Research$$b9$$eCollaboration Author
000283067 773__ $$0PERI:(DE-600)2201940-6$$a10.1002/alz70856_100192$$gVol. 21 Suppl 2, no. Suppl 2, p. e100192$$nSuppl 2$$pe100192$$tAlzheimer's and dementia$$v21$$x1552-5260$$y2025
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