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@ARTICLE{Schneider:277323,
      author       = {Schneider, Luisa Sophie and Freiesleben, Silka Dawn and van
                      Breukelen, Gerard and Wang, Xiao and Brosseron, Frederic and
                      Heneka, Michael T and Teipel, Stefan and Kleineidam, Luca
                      and Stark, Melina and Roy-Kluth, Nina and Wagner, Michael
                      and Spottke, Annika and Schmid, Matthias and Roeske, Sandra
                      and Laske, Christoph and Munk, Matthias H and Perneczky,
                      Robert and Rauchmann, Boris Stephan and Buerger, Katharina
                      and Janowitz, Daniel and Düzel, Emrah and Glanz, Wenzel and
                      Jessen, Frank and Rostamzadeh, Ayda and Wiltfang, Jens and
                      Bartels, Claudia and Kilimann, Ingo and Schneider, Anja and
                      Fliessbach, Klaus and Priller, Josef and Spruth, Eike Jakob
                      and Hellmann-Regen, Julian and Peters, Oliver},
      title        = {{L}inking higher amyloid beta 1-38 ({A}β(1-38)) levels to
                      reduced {A}lzheimer's disease progression risk.},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {2},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2025-00385},
      pages        = {e14545},
      year         = {2025},
      abstract     = {The beneficial effects of amyloid beta 1-38, or Aβ(1-38),
                      on Alzheimer's disease (AD) progression in humans in vivo
                      remain controversial. We investigated AD patients'
                      cerebrospinal fluid (CSF) Aβ(1-38) and AD
                      progression.Cognitive function and diagnostic change were
                      assessed annually for 3 years in 177 Aβ-positive
                      participants with subjective cognitive decline (SCD), mild
                      cognitive impairment (MCI), and dementia from the German
                      Center for Neurodegenerative Diseases (DZNE) longitudinal
                      cognitive impairment and dementia study (DELCODE) cohort
                      using the Mini-Mental State Examination (MMSE), Preclinical
                      Alzheimer's Cognitive Composite (PACC), Clinical Dementia
                      Rating (CDR), and National Institute of Neurological and
                      Communicative Disorders and Stroke-Alzheimer's Disease and
                      Related Disorders Association (NINCDS-ADRDA) criteria. Mixed
                      linear and Cox regression analyses were conducted. CSF was
                      collected at baseline.Higher Aβ(1-38) levels were
                      associated with slower PACC (p = 0.001) and slower CDR Sum
                      of Boxes (CDR-SB) (p = 0.002) but not MMSE decline.
                      Including Aβ(1-40) beyond Aβ(1-38) in the model confirmed
                      an association of Aβ(1-38) with slower PACC decline (p =
                      0.005), but not with CDR-SB or MMSE decline. In addition,
                      higher Aβ(1-38) baseline levels were associated with a
                      reduced dementia conversion risk.Further research is needed
                      to understand the role of Aβ(1-38) in AD and its potential
                      for future therapeutic strategies.This study not only
                      replicates but also extends the existing findings on the
                      role of Aβ(1-38) (amyloid beta 1-38) in Alzheimer's disease
                      (AD) in humans in vivo. Higher baseline Aβ(1-38) levels
                      were associated with a decreased risk of conversion to AD
                      dementia in subjective cognitive decline (SCD) and mild
                      cognitive impairment (MCI). Different linear-mixed
                      regression models suggest an association between higher
                      Aβ(1-38) baseline levels and slower Preclinical Alzheimer's
                      Cognitive Composite (PACC) and Clinical Dementia Rating Sum
                      of Boxes (CDR-SB) decline. Including Aβ(1-40) beyond
                      Aβ(1-38) in the model confirmed a link between Aβ(1-38)
                      and PACC decline, but showed no association of Aβ(1-38) on
                      CDR-SB and Mini-Mental State Examination (MMSE) decline. The
                      impact of short Aβ isoforms in AD progression might have
                      been under-investigated These findings underscore the urgent
                      need for additional research on the role of these shorter
                      Aβ peptides in AD, as they may hold key insights for future
                      therapeutic strategies.},
      keywords     = {Humans / Amyloid beta-Peptides: cerebrospinal fluid /
                      Alzheimer Disease: cerebrospinal fluid / Disease Progression
                      / Male / Female / Peptide Fragments: cerebrospinal fluid /
                      Aged / Cognitive Dysfunction: cerebrospinal fluid /
                      Longitudinal Studies / Mental Status and Dementia Tests /
                      Biomarkers: cerebrospinal fluid / Middle Aged / Aged, 80 and
                      over / Neuropsychological Tests: statistics $\&$ numerical
                      data / AD conversion risk (Other) / Alzheimer's disease
                      (Other) / Aβ(1‐38) (Other) / cerebrospinal fluid (Other)
                      / cognitive decline (Other) / neurotoxicity (Other) /
                      protective factor (Other) / shorter Aβ peptides (Other) /
                      Amyloid beta-Peptides (NLM Chemicals) / Peptide Fragments
                      (NLM Chemicals) / amyloid beta-protein (1-38) (NLM
                      Chemicals) / Biomarkers (NLM Chemicals)},
      cin          = {AG Peters / AG Dirnagl / AG Wagner / AG Spottke / AG Heneka
                      / AG Schmid Bonn / AG Gasser / AG Dichgans / Clinical
                      Research (Munich) / AG Endres / AG Priller / Patient Studies
                      (Bonn) / AG Wiltfang / AG Jessen / AG Düzel},
      ddc          = {610},
      cid          = {I:(DE-2719)5000000 / I:(DE-2719)1810002 /
                      I:(DE-2719)1011201 / I:(DE-2719)1011103 / I:(DE-2719)1011303
                      / I:(DE-2719)1013028 / I:(DE-2719)1210000 /
                      I:(DE-2719)5000022 / I:(DE-2719)1111015 / I:(DE-2719)1811005
                      / I:(DE-2719)5000007 / I:(DE-2719)1011101 /
                      I:(DE-2719)1410006 / I:(DE-2719)1011102 /
                      I:(DE-2719)5000006},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39868793},
      pmc          = {pmc:PMC11863357},
      doi          = {10.1002/alz.14545},
      url          = {https://pub.dzne.de/record/277323},
}