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@ARTICLE{Seemiller:904374,
      author       = {Seemiller, Joseph and Bischof, Gerard Nisal and Hönig,
                      Merle and Tahmasian, Masoud and van Eimeren, Thilo and
                      Drzezga, Alexander and Initiative, the Alzheimer’s Disease
                      Neuroimaging},
      title        = {{I}ndication of retrograde tau spreading along {B}raak
                      stages and functional connectivity pathways},
      journal      = {European journal of nuclear medicine and molecular imaging},
      volume       = {48},
      number       = {7},
      issn         = {0340-6997},
      address      = {Heidelberg [u.a.]},
      publisher    = {Springer-Verl.},
      reportid     = {FZJ-2021-05944},
      pages        = {2272 - 2282},
      year         = {2021},
      abstract     = {Purpose: Tau pathology progression in Alzheimer's disease
                      (AD) is explained through the network degeneration
                      hypothesis and the neuropathological Braak stages; however,
                      the compatibility of these models remains unclear.Methods:
                      We utilized [18F]AV-1451 tau-PET scans of 39 subjects with
                      AD and 39 sex-matched amyloid-negative healthy controls (HC)
                      in the ADNI (Alzheimer's Disease Neuroimaging Initiative)
                      dataset. The peak cluster of tau-tracer uptake was
                      identified in each Braak stage of neuropathological tau
                      deposition and used to create a seed-based functional
                      connectivity network (FCN) using 198 HC subjects, to
                      identify healthy networks unaffected by
                      neurodegeneration.Results: Voxel-wise tau deposition was
                      both significantly higher inside relative to outside FCNs
                      and correlated significantly and positively with levels of
                      healthy functional connectivity. Within many isolated Braak
                      stages and regions, the correlation between tau and
                      intrinsic functional connectivity was significantly stronger
                      than it was across the whole brain. In this way, each peak
                      cluster of tau was related to multiple Braak stages
                      traditionally associated with both earlier and later stages
                      of disease.Conclusion: We show specificity of healthy FCN
                      topography for AD-pathological tau as well as positive
                      voxel-by-voxel correlations between pathological tau and
                      healthy functional connectivity. We propose a model of "up-
                      and downstream" functional tau progression, suggesting that
                      tau pathology evolves along functional connectivity networks
                      not only "downstream" (i.e., along the expected sequence of
                      the established Braak stages) but also in part "upstream" or
                      "retrograde" (i.e., against the expected sequence of the
                      established Braak stages), with pathology in earlier Braak
                      stages intensified by its functional relationship to later
                      disease stages.Keywords: Alzheimer’s disease; Braak stage;
                      Functional connectivity; Network degeneration hypothesis;
                      PET; Tau.},
      cin          = {INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525) / 5254 - Neuroscientific
                      Data Analytics and AI (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253 / G:(DE-HGF)POF4-5254},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {33462630},
      UT           = {WOS:000608658400001},
      doi          = {10.1007/s00259-020-05183-1},
      url          = {https://juser.fz-juelich.de/record/904374},
}