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@INPROCEEDINGS{zl:283117,
      author       = {Özlü, Serap and Grazia, Alice and Dyrba, Martin and
                      Brosseron, Frederic and Buerger, Katharina and Düzel, Emrah
                      and Hellmann-Regen, Julian David Nicolai and Jessen, Frank
                      and Kleineidam, Luca and Laske, Christoph and Perneczky,
                      Robert and Peters, Oliver and Priller, Josef and Ramirez,
                      Alfredo and Schneider, Anja and Spottke, Annika and
                      Synofzik, Matthis and Wiltfang, Jens and Teipel, Stefan},
      title        = {{CSF} {B}iomarkers of {N}euroinflammation in {P}rediction
                      of {B}rain {A}trophy},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {S7},
      issn         = {1552-5260},
      reportid     = {DZNE-2026-00013},
      pages        = {e108159},
      year         = {2025},
      abstract     = {BackgroundInflammation is recognized as a key hallmark of
                      Alzheimer’s disease (AD), alongside amyloid beta (Aβ)
                      accumulation and tau pathology. Recent evidence suggests
                      that neuroinflammatory markers in cerebrospinal fluid (CSF)
                      are associated with progressive neurodegeneration and
                      regional brain atrophy. In this study, we investigated the
                      relationship between CSF inflammatory markers and atrophy in
                      the basal forebrain and hippocampus longitudinally.MethodWe
                      included 296 participants (37 with AD dementia, 69 with mild
                      cognitive impairment (MCI), 98 with subjective cognitive
                      decline (SCD) and 92 healthy control) from the DELCODE
                      study. Data included baseline CSF markers, the
                      Aβ42-phosphotau181 ratio, disease diagnosis, ApoE4 status,
                      and longitudinal structural MRI volumes for specific brain
                      regions, with a mean follow-up of 19.8 months (SD = 16.7).
                      Latent factors were previously derived via Bayesian
                      confirmatory factor analysis from 14 CSF markers and
                      classified into Synaptic, Microglia, Chemokine/Cytokine, and
                      Complement groups. We used linear mixed-effects models to
                      assess interactions between latent factors and time on brain
                      regions-controlling for age, sex, education and ApoE4
                      status- and, based on our systematic review, examined
                      whether neurogranin, sTREM2, ferritin, and YKL40 predicted
                      longitudinal changes.ResultOur findings revealed significant
                      interaction effects between specific biomarkers and regional
                      brain atrophy. Longitudinal atrophy in the hippocampus was
                      significantly associated with higher levels of the synaptic
                      marker (β = -0.018, p = 0.004), sTREM2 (β = -0.012, p =
                      0.031), and YKL40 (β = -0.022, p = 0.0002). Similarly,
                      increased levels of ferritin (β = -0.040, p = 0.024) and
                      YKL40 (β = -0.041, p = 0.029) were predictive of
                      longitudinal atrophy in the basal forebrain. In contrast,
                      neurogranin and other latent factors—including microglia,
                      chemokine/cytokine, and complement—did not show
                      significant associations with atrophy in either brain
                      region.ConclusionThese results suggest that certain
                      biomarkers, particularly the synaptic latent factor and the
                      individual markers sTREM2, ferritin, and YKL40, are
                      predictive of longitudinal neurodegeneration in key brain
                      regions vulnerable to Alzheimer's disease. The associations
                      found with hippocampal and basal forebrain atrophy highlight
                      the potential of these markers for tracking disease
                      progression and improving early detection strategies.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      cin          = {AG Teipel / AG Heneka / Clinical Research (Munich) / AG
                      Düzel / AG Jessen / AG Wagner / AG Gasser / AG Dichgans /
                      AG Priller / Patient Studies (Bonn) / AG Schneider / AG
                      Spottke / AG Wiltfang},
      ddc          = {610},
      cid          = {I:(DE-2719)1510100 / I:(DE-2719)1011303 /
                      I:(DE-2719)1111015 / I:(DE-2719)5000006 / I:(DE-2719)1011102
                      / I:(DE-2719)1011201 / I:(DE-2719)1210000 /
                      I:(DE-2719)5000022 / I:(DE-2719)5000007 / I:(DE-2719)1011101
                      / I:(DE-2719)1011305 / I:(DE-2719)1011103 /
                      I:(DE-2719)1410006},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      doi          = {10.1002/alz70861_108159},
      url          = {https://pub.dzne.de/record/283117},
}