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@ARTICLE{Yildirim:256452,
      author       = {Yildirim, Zerrin and Delen, Firuze and Berron, David and
                      Baumeister, Hannah and Ziegler, Gabriel and Schütze,
                      Hartmut and Glanz, Wenzel and Dobisch, Laura and Peters,
                      Oliver and Freiesleben, Silka Dawn and Schneider,
                      Luisa-Sophie and Priller, Josef and Spruth, Eike Jakob and
                      Schneider, Anja and Fliessbach, Klaus and Wiltfang, Jens and
                      Schott, Björn-Hendrik and Meiberth, Dix and Buerger,
                      Katharina and Janowitz, Daniel and Perneczky, Robert and
                      Rauchmann, Boris Stephan and Teipel, Stefan and Kilimann,
                      Ingo and Laske, Christoph and Munk, Matthias H and Spottke,
                      Annika and Roy, Nina and Heneka, Michael and Brosseron,
                      Frederic and Wagner, Michael and Roeske, Sandra and Ramirez,
                      Alfredo and Ewers, Michael and Dechent, Peter and Hetzer,
                      Stefan and Scheffler, Klaus and Kleineidam, Luca and
                      Wolfsgruber, Steffen and Yakupov, Renat and Schmid, Matthias
                      and Berger, Moritz and Gurvit, Hakan and Jessen, Frank and
                      Duzel, Emrah},
      title        = {{B}rain reserve contributes to distinguishing preclinical
                      {A}lzheimer's stages 1 and 2.},
      journal      = {Alzheimer's research $\&$ therapy},
      volume       = {15},
      number       = {1},
      issn         = {1758-9193},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DZNE-2023-00314},
      pages        = {43},
      year         = {2023},
      note         = {CC BY},
      abstract     = {In preclinical Alzheimer's disease, it is unclear why some
                      individuals with amyloid pathologic change are asymptomatic
                      (stage 1), whereas others experience subjective cognitive
                      decline (SCD, stage 2). Here, we examined the association of
                      stage 1 vs. stage 2 with structural brain reserve in
                      memory-related brain regions.We tested whether the volumes
                      of hippocampal subfields and parahippocampal regions were
                      larger in individuals at stage 1 compared to asymptomatic
                      amyloid-negative older adults (healthy controls, HCs). We
                      also tested whether individuals with stage 2 would show the
                      opposite pattern, namely smaller brain volumes than in
                      amyloid-negative individuals with SCD. Participants with
                      cerebrospinal fluid (CSF) biomarker data and bilateral
                      volumetric MRI data from the observational, multi-centric
                      DZNE-Longitudinal Cognitive Impairment and Dementia Study
                      (DELCODE) study were included. The sample comprised 95
                      amyloid-negative and 26 amyloid-positive asymptomatic
                      participants as well as 104 amyloid-negative and 47
                      amyloid-positive individuals with SCD. Volumes were based on
                      high-resolution T2-weighted images and automatic
                      segmentation with manual correction according to a recently
                      established high-resolution segmentation protocol.In
                      asymptomatic individuals, brain volumes of hippocampal
                      subfields and of the parahippocampal cortex were numerically
                      larger in stage 1 compared to HCs, whereas the opposite was
                      the case in individuals with SCD. MANOVAs with volumes as
                      dependent data and age, sex, years of education, and DELCODE
                      site as covariates showed a significant interaction between
                      diagnosis (asymptomatic versus SCD) and amyloid status
                      (Aß42/40 negative versus positive) for hippocampal
                      subfields. Post hoc paired comparisons taking into account
                      the same covariates showed that dentate gyrus and CA1
                      volumes in SCD were significantly smaller in
                      amyloid-positive than negative individuals. In contrast, CA1
                      volumes were significantly (p = 0.014) larger in stage 1
                      compared with HCs.These data indicate that HCs and stages 1
                      and 2 do not correspond to linear brain volume reduction.
                      Instead, stage 1 is associated with larger than expected
                      volumes of hippocampal subfields in the face of amyloid
                      pathology. This indicates a brain reserve mechanism in stage
                      1 that enables individuals with amyloid pathologic change to
                      be cognitively normal and asymptomatic without subjective
                      cognitive decline.},
      keywords     = {Humans / Aged / Alzheimer Disease: diagnostic imaging /
                      Cognitive Reserve / Amyloidogenic Proteins / Cerebral Cortex
                      / Cognitive Dysfunction: diagnostic imaging / Alzheimer’s
                      disease (AD) (Other) / Amyloid pathologic change (Other) /
                      Aß42/40 (Other) / Brain reserve (Other) / Cerebrospinal
                      fluid (CSF) (Other) / Hippocampus (Other) / Magnetic
                      resonance imaging (MRI) (Other) / Medial temporal lobe
                      (Other) / Memory (Other) / Subjective cognitive decline
                      (SCD) (Other) / Amyloidogenic Proteins (NLM Chemicals)},
      cin          = {AG Düzel / AG Berron / KAP / AG Dirnagl / AG Priller / AG
                      Endres / AG Schneider / Patient Studies Bonn / AG Jessen /
                      AG Wiltfang / AG Fischer / AG Dichgans / AG Teipel / AG
                      Gasser / Clinical Research Platform (CRP) / Biomarker / AG
                      Wagner / AG Simons / AG Schmid Bonn / Delcode},
      ddc          = {610},
      cid          = {I:(DE-2719)5000006 / I:(DE-2719)5000070 /
                      I:(DE-2719)1340013 / I:(DE-2719)1810002 / I:(DE-2719)5000007
                      / I:(DE-2719)1811005 / I:(DE-2719)1011305 /
                      I:(DE-2719)1011101 / I:(DE-2719)1011102 / I:(DE-2719)1410006
                      / I:(DE-2719)1410002 / I:(DE-2719)5000022 /
                      I:(DE-2719)1510100 / I:(DE-2719)1210000 / I:(DE-2719)1011401
                      / I:(DE-2719)1011301 / I:(DE-2719)1011201 /
                      I:(DE-2719)1110008 / I:(DE-2719)1013028 /
                      I:(DE-2719)5000034},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352) / 351 - Brain Function
                      (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-351},
      experiment   = {EXP:(DE-2719)DELCODE-20140101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36855049},
      pmc          = {pmc:PMC9972621},
      doi          = {10.1186/s13195-023-01187-9},
      url          = {https://pub.dzne.de/record/256452},
}