% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Heinzinger:256606,
      author       = {Heinzinger, Nils and Maass, Anne and Berron, David and
                      Yakupov, Renat and Peters, Oliver and Fiebach, Jochen and
                      Villringer, Kersten and Preis, Lukas and Priller, Josef and
                      Spruth, Eike Jacob and Altenstein, Slawek and Schneider,
                      Anja and Fliessbach, Klaus and Wiltfang, Jens and Bartels,
                      Claudia and Jessen, Frank and Maier, Franziska and Glanz,
                      Wenzel and Buerger, Katharina and Janowitz, Daniel and
                      Perneczky, Robert and Rauchmann, Boris Stephan and Teipel,
                      Stefan and Killimann, Ingo and Göerß, Doreen and Laske,
                      Christoph and Munk, Matthias H and Spottke, Annika and Roy,
                      Nina and Heneka, Michael T and Brosseron, Frederic and
                      Dobisch, Laura and Ewers, Michael and Dechent, Peter and
                      Haynes, John Dylan and Scheffler, Klaus and Wolfsgruber,
                      Steffen and Kleineidam, Luca and Schmid, Matthias and
                      Berger, Moritz and Düzel, Emrah and Ziegler, Gabriel},
      collaboration = {Initiative, Alzheimer’s Disease Neuroimaging},
      title        = {{E}xploring the {ATN} classification system using brain
                      morphology.},
      journal      = {Alzheimer's research $\&$ therapy},
      volume       = {15},
      number       = {1},
      issn         = {1758-9193},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DZNE-2023-00358},
      pages        = {50},
      year         = {2023},
      note         = {CC BY},
      abstract     = {The NIA-AA proposed amyloid-tau-neurodegeneration (ATN) as
                      a classification system for AD biomarkers. The amyloid
                      cascade hypothesis (ACH) implies a sequence across ATN
                      groups that patients might undergo during transition from
                      healthy towards AD: A-T-N-➔A+T-N-➔A+T+N-➔A+T+N+. Here
                      we assess the evidence for monotonic brain volume decline
                      for this particular (amyloid-conversion first,
                      tau-conversion second, N-conversion last) and alternative
                      progressions using voxel-based morphometry (VBM) in a large
                      cross-sectional MRI cohort.We used baseline data of the
                      DELCODE cohort of 437 subjects (127 controls, 168 SCD, 87
                      MCI, 55 AD patients) which underwent lumbar puncture, MRI
                      scanning, and neuropsychological assessment. ATN
                      classification was performed using CSF-Aβ42/Aβ40 (A+/-),
                      CSF phospho-tau (T+/-), and adjusted hippocampal volume or
                      CSF total-tau (N+/-). We compared voxel-wise model evidence
                      for monotonic decline of gray matter volume across various
                      sequences over ATN groups using the Bayesian Information
                      Criterion (including also ROIs of Braak stages). First, face
                      validity of the ACH transition sequence
                      A-T-N-➔A+T-N-➔A+T+N-➔A+T+N+ was compared against
                      biologically less plausible (permuted) sequences among AD
                      continuum ATN groups. Second, we evaluated evidence for 6
                      monotonic brain volume progressions from A-T-N- towards
                      A+T+N+ including also non-AD continuum ATN groups.The
                      ACH-based progression A-T-N-➔A+T-N-➔A+T+N-➔A+T+N+ was
                      consistent with cognitive decline and clinical diagnosis.
                      Using hippocampal volume for operationalization of
                      neurodegeneration (N), ACH was most evident in $9\%$ of gray
                      matter predominantly in the medial temporal lobe. Many
                      cortical regions suggested alternative non-monotonic volume
                      progressions over ACH progression groups, which is
                      compatible with an early amyloid-related tissue expansion or
                      sampling effects, e.g., due to brain reserve. Volume decline
                      in $65\%$ of gray matter was consistent with a progression
                      where A status converts before T or N status (i.e., ACH/ANT)
                      when compared to alternative sequences (TAN/TNA/NAT/NTA).
                      Brain regions earlier affected by tau tangle deposition
                      (Braak stage I-IV, MTL, limbic system) present stronger
                      evidence for volume decline than late Braak stage ROIs
                      (V/VI, cortical regions). Similar findings were observed
                      when using CSF total-tau for N instead.Using the ATN
                      classification system, early amyloid status conversion
                      (before tau and neurodegeneration) is associated with brain
                      volume loss observed during AD progression. The ATN system
                      and the ACH are compatible with monotonic progression of MTL
                      atrophy.DRKS00007966, 04/05/2015, retrospectively
                      registered.},
      subtyp        = {Review Article},
      keywords     = {Humans / Alzheimer Disease: diagnostic imaging /
                      Cross-Sectional Studies / Bayes Theorem / Amyloid
                      beta-Peptides / Cognitive Dysfunction: diagnostic imaging /
                      Brain: diagnostic imaging / Amyloidogenic Proteins / tau
                      Proteins / Biomarkers / Alzheimer’s disease (Other) / ATN
                      (Other) / Alzheimer’s disease (Other) / Amyloid (Other) /
                      Biomarker (Other) / MRI (Other) / Memory (Other) / VBM
                      (Other) / Voxel-based morphometry (Other) / Amyloid
                      beta-Peptides (NLM Chemicals) / Amyloidogenic Proteins (NLM
                      Chemicals) / tau Proteins (NLM Chemicals) / Biomarkers (NLM
                      Chemicals)},
      cin          = {AG Düzel / AG Maaß / AG Berron / AG Dirnagl / AG Priller
                      / AG Endres / AG Schneider / Patient Studies Bonn / AG
                      Wiltfang / AG Jessen / AG Dichgans / AG Gasser / Clinical
                      Research Platform (CRP) / AG Teipel / Biomarker / AG Simons
                      / AG Wagner / AG Schmid Bonn},
      ddc          = {610},
      cid          = {I:(DE-2719)5000006 / I:(DE-2719)1311001 /
                      I:(DE-2719)5000070 / I:(DE-2719)1810002 / I:(DE-2719)5000007
                      / I:(DE-2719)1811005 / I:(DE-2719)1011305 /
                      I:(DE-2719)1011101 / I:(DE-2719)1410006 / I:(DE-2719)1011102
                      / I:(DE-2719)5000022 / I:(DE-2719)1210000 /
                      I:(DE-2719)1011401 / I:(DE-2719)1510100 / I:(DE-2719)1011301
                      / I:(DE-2719)1110008 / I:(DE-2719)1011201 /
                      I:(DE-2719)1013028},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 351 -
                      Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-351},
      experiment   = {EXP:(DE-2719)DELCODE-20140101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36915139},
      pmc          = {pmc:PMC10009950},
      doi          = {10.1186/s13195-023-01185-x},
      url          = {https://pub.dzne.de/record/256606},
}