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@ARTICLE{Lee:154260,
      author       = {Lee, Hwee Ling and Stirnberg, Rüdiger and Wu, Sichu and
                      Wang, Xin and Stöcker, Tony and Jung, Sonja and Montag,
                      Christian and Axmacher, Nikolai},
      title        = {{G}enetic {A}lzheimer's {D}isease {R}isk {A}ffects the
                      {N}eural {M}echanisms of {P}attern {S}eparation in
                      {H}ippocampal {S}ubfields.},
      journal      = {Current biology},
      volume       = {30},
      number       = {21},
      issn         = {0960-9822},
      address      = {London},
      publisher    = {Current Biology Ltd.},
      reportid     = {DZNE-2021-00114},
      pages        = {4201 - 4212.e3},
      year         = {2020},
      note         = {ISSN 0960-9822 not unique: **3 hits**.},
      abstract     = {The hippocampal subfields perform distinct operations
                      during acquisition, differentiation, and recollection of
                      episodic memories, and deficits in pattern separation are
                      among the first symptoms of Alzheimer's disease (AD). We
                      investigated how hippocampal subfields contribute to pattern
                      separation and how this is affected by Apolipoprotein-E
                      (APOE), the strongest AD genetic risk factor. Using
                      ultra-high-field (7T) functional magnetic resonance imaging
                      (fMRI), APOE-ε3-ε3 carriers predominantly recruited cornu
                      ammonis 3 (CA3) during a spatial mnemonic discrimination
                      task, whereas APOE-ε3-ε4 and APOE-ε3-ε2 carriers engaged
                      CA3 and dentate gyrus (DG) to the same degree. Specifically,
                      APOE-ε3-ε4 carriers showed reduced pattern separation in
                      CA3, whereas APOE-ε3-ε2 carriers exhibited increased
                      effects in DG and pattern separation-related functional
                      connectivity between DG and CA3. Collectively, these results
                      demonstrate that AD genetic risk alters hemodynamic
                      responses in young pre-symptomatic individuals, paving the
                      way for development of biomarkers for preclinical AD.},
      keywords     = {Adult / Alleles / Alzheimer Disease: diagnosis / Alzheimer
                      Disease: genetics / Alzheimer Disease: physiopathology /
                      Apolipoproteins E: genetics / Apolipoproteins E: metabolism
                      / Brain Mapping / CA3 Region, Hippocampal: diagnostic
                      imaging / CA3 Region, Hippocampal: physiopathology / Dentate
                      Gyrus: diagnostic imaging / Dentate Gyrus: physiopathology /
                      Female / Genetic Predisposition to Disease / Genotyping
                      Techniques / Healthy Volunteers / Heterozygote / Humans /
                      Magnetic Resonance Imaging / Male / Memory, Episodic / Risk
                      Factors / Young Adult / 7T (Other) / APOE genotype (Other) /
                      CA3 (Other) / dentate gyrus (Other) / episodic memory
                      (Other) / functional connectivity (Other) / hippocampal
                      subfields (Other) / pattern separation (Other)},
      cin          = {Patient studies, Bonn / AG Stöcker / AG Axmacher},
      ddc          = {570},
      cid          = {I:(DE-2719)1011101 / I:(DE-2719)1013026 /
                      I:(DE-2719)5000027},
      pnm          = {344 - Clinical and Health Care Research (POF3-344) / 345 -
                      Population Studies and Genetics (POF3-345)},
      pid          = {G:(DE-HGF)POF3-344 / G:(DE-HGF)POF3-345},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32916120},
      doi          = {10.1016/j.cub.2020.08.042},
      url          = {https://pub.dzne.de/record/154260},
}