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@ARTICLE{Steward:165602,
      author       = {Steward, Anna and Biel, Davina and Brendel, Matthias and
                      Dewenter, Anna and Roemer, Sebastian and Rubinski, Anna and
                      Luan, Ying and Dichgans, Martin and Ewers, Michael and
                      Franzmeier, Nicolai},
      collaboration = {Initiative, Alzheimer's Disease Neuroimaging},
      title        = {{F}unctional network segregation is associated with
                      attenuated tau spreading in {A}lzheimer's disease.},
      journal      = {Alzheimer's and dementia},
      volume       = {19},
      number       = {5},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2022-01735},
      pages        = {2034-2046},
      year         = {2023},
      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.},
      keywords     = {Humans / Alzheimer Disease: pathology / Amyloid
                      beta-Peptides: metabolism / Brain: pathology / Cognitive
                      Dysfunction: pathology / Connectome: methods / Magnetic
                      Resonance Imaging: methods / Positron-Emission Tomography /
                      tau Proteins: metabolism / Amyloid beta-Peptides (NLM
                      Chemicals) / Alzheimer's disease (Other) / functional
                      magnetic resonance imaging (Other) / network segregation
                      (Other) / tau positron emission tomography (Other) / tau
                      spreading (Other) / tau Proteins (NLM Chemicals)},
      cin          = {AG Haass old ; AG Haass / AG Dichgans / AG Simons},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007 / I:(DE-2719)5000022 /
                      I:(DE-2719)1110008},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352) / 351 - Brain Function
                      (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36433865},
      doi          = {10.1002/alz.12867},
      url          = {https://pub.dzne.de/record/165602},
}