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@INPROCEEDINGS{Dzel:283043,
      author       = {Düzel, Emrah and Cikrikcili, Ugur and Schott, Björn H.
                      and Jockschat, Thomas Nickl and Berron, David and Soch,
                      Joram and Krohn, Friedrich},
      title        = {{A}mygdala {N}ovelty {R}esponses, {D}epressive {S}ymptoms,
                      and {T}au {P}athology in {P}reclinical {A}lzheimer's
                      {D}isease: {A}n f{MRI} {I}nvestigation},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {S1},
      issn         = {1552-5260},
      reportid     = {DZNE-2025-01450},
      pages        = {e107337},
      year         = {2025},
      abstract     = {Background: Late-life depression (LLD) is a
                      well-established risk factor for Alzheimer's disease (AD)
                      and has been linked to cognitive decline. The amygdala, an
                      important region for emotional regulation and novelty
                      detection, is one of the earliest sites of tau accumulation
                      in AD. However, it remains unclear how depressive symptoms
                      and tau burden interact with amygdala function in
                      preclinical AD stages. This study examines the relationship
                      between amygdala novelty responses, depressive
                      symptoms.Method:A total of 190 participants (HC = 58, SCD =
                      88, MCI = 44) underwent functional MRI (fMRI) to assess
                      amygdala novelty responses. Depression severity was measured
                      using the GDS, and tau pathology was classified based on CSF
                      phosphorylated tau (p-Tau) and total tau (t-Tau) levels.
                      Participants were further categorized based on depressive
                      symptoms (GDS = 0 vs. GDS ≥1) and tau status (Tau (-) vs.
                      Tau (+)) for statistical analyses.Result:Group comparisons
                      revealed significantly higher GDS scores in SCD and MCI
                      groups compared to HC (p < 0.05), reflecting increased
                      depressive symptoms in individuals with cognitive
                      complaints. However, no significant correlation was observed
                      between amygdala novelty responses and GDS scores across
                      diagnostic groups. Additionally, CSF tau levels (p-Tau and
                      t-Tau) did not significantly interact with depressive
                      symptoms in predicting amygdala responses. The lack of
                      significant findings in amygdala response may be attributed
                      to the relatively low overall severity of depressive
                      symptoms in the sample, which could limit detectability of
                      neural alterations.Conclusion: Although prior studies have
                      indicated that late-life depression and tau pathology are
                      associated with the progression of Alzheimer's disease (AD),
                      our findings suggest that subclinical depressive symptoms do
                      not significantly impact amygdala novelty responses in
                      preclinical AD. The observed increase in depressive symptoms
                      in SCD and MCI groups suggests that affective changes may
                      still be an important factor in disease progression, but
                      their relationship with amygdala function remains unclear.
                      Future research should explore clinically significant
                      depression, longitudinal changes in affective symptoms, and
                      other neurobiological mechanisms, such as amyloid burden and
                      neuroinflammation, to better understand the early neural
                      changes associated with AD.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      keywords     = {Humans / Male / Female / Amygdala: physiopathology /
                      Amygdala: diagnostic imaging / Magnetic Resonance Imaging /
                      tau Proteins: cerebrospinal fluid / Aged / Depression:
                      physiopathology / Cognitive Dysfunction: physiopathology /
                      Cognitive Dysfunction: diagnostic imaging / Alzheimer
                      Disease / Middle Aged / tau Proteins (NLM Chemicals)},
      cin          = {AG Düzel / AG Fischer / AG Berron / Clinical Dementia
                      Research (Göttingen)},
      ddc          = {610},
      cid          = {I:(DE-2719)5000006 / I:(DE-2719)1410002 /
                      I:(DE-2719)5000070 / I:(DE-2719)1440015},
      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)1 / PUB:(DE-HGF)16},
      doi          = {10.1002/alz70855_107337},
      url          = {https://pub.dzne.de/record/283043},
}