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@ARTICLE{Wang:272342,
      author       = {Wang, Xiao and Freiesleben, Silka Dawn and Schneider,
                      Luisa-Sophie and Preis, Lukas and Priller, Josef and Spruth,
                      Eike Jakob and Altenstein, Slawek and Schneider, Anja and
                      Fließbach, Klaus and Wiltfang, Jens and Hansen, Niels and
                      Jessen, Frank and Rostamzadeh, Ayda and Duzel, Emrah and
                      Glanz, Wenzel and Incesoy, Enise I and Bürger, Katharina
                      and Janowitz, Daniel and Ewers, Michael and Perneczky,
                      Robert and Rauchmann, Boris Stephan and Teipel, Stefan J and
                      Kilimann, Ingo and Goerss, Doreen and Laske, Christoph and
                      Munk, Matthias H J and Spottke, Annika and Roy, Nina and
                      Heneka, Michael and Brosseron, Frederic and Wagner, Michael
                      and Wolfsgruber, Steffen and Ramirez, Alfredo and
                      Kleineidam, Luca and Stark, Melina and Peters, Oliver},
      title        = {{A}ssociation of {N}eurogranin and {BACE}1 {W}ith
                      {C}linical {C}ognitive {D}ecline in {I}ndividuals {W}ith
                      {S}ubjective {C}ognitive {D}ecline.},
      journal      = {Neurology},
      volume       = {103},
      number       = {8},
      issn         = {0028-3878},
      address      = {[Erscheinungsort nicht ermittelbar]},
      publisher    = {Ovid},
      reportid     = {DZNE-2024-01159},
      pages        = {e209806},
      year         = {2024},
      abstract     = {CSF biomarkers have immense diagnostic and prognostic
                      potential for Alzheimer disease (AD). However, AD is still
                      diagnosed relatively late in the disease process, sometimes
                      even years after the initial manifestation of cognitive
                      symptoms. Thus, further identification of biomarkers is
                      required to detect related pathology in the preclinical
                      stage and predict cognitive decline. Our study aimed to
                      assess the association of neurogranin and β-site amyloid
                      precursor protein-cleaving enzyme 1 (BACE1) with cognitive
                      decline in individuals with subjective cognitive decline
                      (SCD).We enrolled participants with available neurogranin
                      and BACE1 measurements in CSF from the DELCODE
                      (DZNE-Longitudinal Cognitive Impairment and Dementia,
                      Germany) cohort. The longitudinal change of Preclinical
                      Alzheimer's Cognitive Composite score was assessed as the
                      primary outcome in participants with SCD and controls. The
                      secondary outcome was defined as conversion of SCD to mild
                      cognitive impairment (MCI) during follow-up. Levels of
                      neurogranin, BACE1, and neurogranin/BACE1 ratio across
                      groups were compared by analysis of covariance after
                      adjustment for demographics. The linear mixed-effects model
                      and Cox regression analysis were applied to evaluate their
                      association with cognitive decline and progression of SCD to
                      MCI, respectively.A total of 530 participants (mean age:
                      70.76 ± 6.01 years, $48.7\%$ female) were analyzed in the
                      study. The rate of cognitive decline was faster in
                      individuals with SCD with higher neurogranin and
                      neurogranin/BACE1 ratio (β = -0.138, SE = 0.065, p = 0.037,
                      and β = -0.293, SE = 0.115, p = 0.013). Higher baseline
                      neurogranin and neurogranin/BACE1 ratio were associated with
                      an increased rate of conversion from SCD to MCI (hazard
                      ratio [HR] 1.35 per SD, $95\%$ CI 1.03-1.77, p = 0.028, and
                      HR 1.53 per SD, $95\%$ CI 1.13-2.07, p = 0.007). In
                      addition, the impact of higher neurogranin levels on
                      accelerating the rate of cognitive decline was more
                      pronounced in the SCD group than in cognitively unimpaired
                      controls (β = -0.077, SE = 0.033, p = 0.020).Our findings
                      suggest that CSF neurogranin and BACE1 begin to change in
                      the preclinical stage of AD and they are associated with
                      clinical progression in individuals with SCD.},
      keywords     = {Humans / Aspartic Acid Endopeptidases: cerebrospinal fluid
                      / Amyloid Precursor Protein Secretases: cerebrospinal fluid
                      / Female / Male / Cognitive Dysfunction: cerebrospinal fluid
                      / Aged / Neurogranin: cerebrospinal fluid / Disease
                      Progression / Biomarkers: cerebrospinal fluid / Longitudinal
                      Studies / Middle Aged / Aged, 80 and over / Aspartic Acid
                      Endopeptidases (NLM Chemicals) / Amyloid Precursor Protein
                      Secretases (NLM Chemicals) / Neurogranin (NLM Chemicals) /
                      BACE1 protein, human (NLM Chemicals) / Biomarkers (NLM
                      Chemicals)},
      cin          = {AG Peters / AG Priller / AG Endres / AG Schneider / Patient
                      Studies (Bonn) / AG Wiltfang / AG Jessen / AG Düzel /
                      Clinical Research (Munich) / AG Dichgans / AG Teipel / AG
                      Gasser / AG Spottke / Clinical Research Platform (CRP) / AG
                      Heneka / AG Wagner},
      ddc          = {610},
      cid          = {I:(DE-2719)5000000 / 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)5000006 / I:(DE-2719)1111015 / I:(DE-2719)5000022
                      / I:(DE-2719)1510100 / I:(DE-2719)1210000 /
                      I:(DE-2719)1011103 / I:(DE-2719)1011401 / I:(DE-2719)1011303
                      / I:(DE-2719)1011201},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39303184},
      doi          = {10.1212/WNL.0000000000209806},
      url          = {https://pub.dzne.de/record/272342},
}