Journal Article

DZNE-2022-01735

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Functional network segregation is associated with attenuated tau spreading in Alzheimer's disease.

Steward, A. ; Biel, D. ; Brendel, M.DZNE* ; Dewenter, A. ; Roemer, S. ; Rubinski, A.Extern* ; Luan, Y. ; Dichgans, M.DZNE* ; Ewers, M.DZNE* ; Franzmeier, N. ; Initiative, A. D. N. (Collaboration Author)

2023
Wiley Hoboken, NJ

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Please use a persistent id in citations: doi:10.1002/alz.12867

Abstract: Lower 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.

Keyword(s): Humans (MeSH) ; Alzheimer Disease: pathology (MeSH) ; Amyloid beta-Peptides: metabolism (MeSH) ; Brain: pathology (MeSH) ; Cognitive Dysfunction: pathology (MeSH) ; Connectome: methods (MeSH) ; Magnetic Resonance Imaging: methods (MeSH) ; Positron-Emission Tomography (MeSH) ; tau Proteins: metabolism (MeSH) ; Amyloid beta-Peptides ; Alzheimer's disease ; functional magnetic resonance imaging ; network segregation ; tau positron emission tomography ; tau spreading ; tau Proteins

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Contributing Institute(s):

1. Molecular Neurodegeneration (AG Haass old ; AG Haass)
2. Vascular Cognitive Impairment & Post-Stroke Dementia (AG Dichgans)
3. Molecular Neurobiology (AG Simons)

Research Program(s):

1. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)
2. 352 - Disease Mechanisms (POF4-352) (POF4-352)
3. 351 - Brain Function (POF4-351) (POF4-351)

Appears in the scientific report 2023

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Database coverage:
; ; ; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; DEAL Wiley ; Essential Science Indicators ; IF >= 10 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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