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001     165602
005     20240112171933.0
024 7 _ |a 10.1002/alz.12867
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024 7 _ |a pmid:36433865
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024 7 _ |a 1552-5260
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024 7 _ |a 1552-5279
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037 _ _ |a DZNE-2022-01735
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Steward, Anna
|b 0
245 _ _ |a Functional network segregation is associated with attenuated tau spreading in Alzheimer's disease.
260 _ _ |a Hoboken, NJ
|c 2023
|b Wiley
336 7 _ |a article
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520 _ _ |a 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.
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650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: pathology
|2 MeSH
650 _ 2 |a Connectome: methods
|2 MeSH
650 _ 2 |a Magnetic Resonance Imaging: methods
|2 MeSH
650 _ 2 |a Positron-Emission Tomography
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Alzheimer's disease
|2 Other
650 _ 7 |a functional magnetic resonance imaging
|2 Other
650 _ 7 |a network segregation
|2 Other
650 _ 7 |a tau positron emission tomography
|2 Other
650 _ 7 |a tau spreading
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650 _ 7 |a tau Proteins
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700 1 _ |a Biel, Davina
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700 1 _ |a Brendel, Matthias
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700 1 _ |a Dewenter, Anna
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700 1 _ |a Roemer, Sebastian
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700 1 _ |a Rubinski, Anna
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700 1 _ |a Luan, Ying
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700 1 _ |a Dichgans, Martin
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700 1 _ |a Ewers, Michael
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700 1 _ |a Franzmeier, Nicolai
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700 1 _ |a Initiative, Alzheimer's Disease Neuroimaging
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773 _ _ |a 10.1002/alz.12867
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