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@ARTICLE{Eckenweber:285360,
      author       = {Eckenweber, Sebastian and Völter, Friederike and
                      Franzmeier, Nicolai and Palleis, Carla and Wagemann, Olivia
                      and Weidinger, Endy and Katzdobler, Sabrina and Wlasich,
                      Elisabeth and Sandkühler, Katja and Böning, Guido and
                      Gnoerich, Johannes and Scheifele, Maximilian and Eckenweber,
                      Florian and Janowitz, Daniel and Kurz, Carolin and
                      Perneczky, Robert and Bürger, Katharina and Danek, Adrian
                      and Höglinger, Günter and Levin, Johannes and Brendel,
                      Matthias and Schönecker, Sonja},
      title        = {{A}dditive value of early-phase β-{A}myloid-{PET} for the
                      differential diagnosis of non-{A}lzheimer's disease
                      dementia.},
      journal      = {NeuroImage: Clinical},
      volume       = {49},
      issn         = {2213-1582},
      address      = {[Amsterdam u.a.]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2026-00225},
      pages        = {103963},
      year         = {2026},
      abstract     = {Recent studies demonstrated strong agreement between
                      early-phase β-amyloid-PET perfusion imaging and glucose
                      hypometabolism assessed by [18F]FDG-PET, indicating the
                      potential of early-phase β-amyloid-PET as a surrogate
                      biomarker of neuronal injury. We therefore aimed to
                      investigate the additive value of early-phase β-amyloid-PET
                      for the differential diagnosis of non-Alzheimer's disease
                      dementia syndromes in clinical routine.[18F]florbetaben- and
                      [18F]flutemetamol-PET scans (n = 379) performed between July
                      2013 and July 2021 were analyzed for their amyloid status
                      and the presence of a neurodegenerative hypoperfusion
                      pattern using visual assessment and z-score maps. In
                      patients visually rated as
                      amyloid-negative/neurodegeneration-positive (A-N+), the most
                      likely diagnosis based on perfusion patterns was compared to
                      the final clinical diagnosis, i.e. frontotemporal dementia
                      or psychiatric disorders, suspected 4R-tauopathy, and
                      suspected non-Alzheimer pathophysiology. Logistic regression
                      models based on a data-driven selection of cerebral regions
                      of hypoperfusion by principal component analysis were used
                      to predict neurodegenerative disease and clinical diagnoses.
                      Diagnostic accuracy was compared between visual assessment
                      and the regression models.Neurodegeneration status was
                      correctly identified in $78.8\%$ (119/151) of
                      amyloid-negative patients through visual rating, compared to
                      $67.5\%$ (102/151) using logistic regression. Visual
                      assessment assigned $75.3\%$ (67/89) of A-N+ patients to the
                      correct diagnostic category. In contrast, the regression
                      model classified $69.7\%$ (62/89) of patients.The current
                      study demonstrates an additive value of early-phase
                      β-amyloid-PET for the differential diagnosis of dementia
                      syndromes. While visual assessment of early-phase
                      β-amyloid-PET already provides substantial diagnostic
                      accuracy, a data-driven analysis approach could aid in cases
                      of uncertainty.},
      keywords     = {4-repeattauopathy (Other) / Data driven (Other) /
                      Early-phaseβ-amyloid-PET (Other) / Frontotemporal dementia
                      (Other) / Multinomial logistic regression (Other) /
                      Suspected non-Alzheimer pathophysiology (Other)},
      cin          = {Clinical Research (Munich) / AG Dichgans / AG Levin / AG
                      Haass},
      ddc          = {610},
      cid          = {I:(DE-2719)1111015 / I:(DE-2719)5000022 /
                      I:(DE-2719)1111016 / I:(DE-2719)1110007},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41690259},
      pmc          = {pmc:PMC12925280},
      doi          = {10.1016/j.nicl.2026.103963},
      url          = {https://pub.dzne.de/record/285360},
}