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000165602 037__ $$aDZNE-2022-01735
000165602 041__ $$aEnglish
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000165602 1001_ $$aSteward, Anna$$b0
000165602 245__ $$aFunctional network segregation is associated with attenuated tau spreading in Alzheimer's disease.
000165602 260__ $$aHoboken, NJ$$bWiley$$c2023
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000165602 520__ $$aLower network segregation is associated with accelerated cognitive decline in Alzheimer's disease (AD), yet it is unclear whether less segregated brain networks facilitate connectivity-mediated tau spreading.We combined resting state functional magnetic resonance imaging (fMRI) with longitudinal tau positron emission tomography (PET) in 42 betamyloid-negative controls and 81 amyloid beta positive individuals across the AD spectrum. Network segregation was determined using resting-state fMRI-assessed connectivity among 400 cortical regions belonging to seven networks.AD subjects with higher network segregation exhibited slower brain-wide tau accumulation relative to their baseline entorhinal tau PET burden (typical onset site of tau pathology). Second, by identifying patient-specific tau epicenters with highest baseline tau PET we found that stronger epicenter segregation was associated with a slower rate of tau accumulation in the rest of the brain in relation to baseline epicenter tau burden.Our results indicate that tau spreading is facilitated by a more diffusely organized connectome, suggesting that brain network topology modulates tau spreading in AD.Higher brain network segregation is associated with attenuated tau pathology accumulation in Alzheimer's disease (AD). A patient-tailored approach allows for the more precise localization of tau epicenters. The functional segregation of subject-specific tau epicenters predicts the rate of future tau accumulation.
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000165602 650_2 $$2MeSH$$aHumans
000165602 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000165602 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000165602 650_2 $$2MeSH$$aBrain: pathology
000165602 650_2 $$2MeSH$$aCognitive Dysfunction: pathology
000165602 650_2 $$2MeSH$$aConnectome: methods
000165602 650_2 $$2MeSH$$aMagnetic Resonance Imaging: methods
000165602 650_2 $$2MeSH$$aPositron-Emission Tomography
000165602 650_2 $$2MeSH$$atau Proteins: metabolism
000165602 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000165602 650_7 $$2Other$$aAlzheimer's disease
000165602 650_7 $$2Other$$afunctional magnetic resonance imaging
000165602 650_7 $$2Other$$anetwork segregation
000165602 650_7 $$2Other$$atau positron emission tomography
000165602 650_7 $$2Other$$atau spreading
000165602 650_7 $$2NLM Chemicals$$atau Proteins
000165602 7001_ $$aBiel, Davina$$b1
000165602 7001_ $$0P:(DE-2719)9001539$$aBrendel, Matthias$$b2$$udzne
000165602 7001_ $$aDewenter, Anna$$b3
000165602 7001_ $$aRoemer, Sebastian$$b4
000165602 7001_ $$0P:(DE-2719)2812415$$aRubinski, Anna$$b5$$udzne
000165602 7001_ $$aLuan, Ying$$b6
000165602 7001_ $$0P:(DE-2719)2000030$$aDichgans, Martin$$b7$$udzne
000165602 7001_ $$0P:(DE-2719)9000543$$aEwers, Michael$$b8$$udzne
000165602 7001_ $$aFranzmeier, Nicolai$$b9
000165602 7001_ $$aInitiative, Alzheimer's Disease Neuroimaging$$b10$$eCollaboration Author
000165602 773__ $$0PERI:(DE-600)2201940-6$$a10.1002/alz.12867$$gp. alz.12867$$n5$$p2034-2046$$tAlzheimer's and dementia$$v19$$x1552-5260$$y2023
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