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@ARTICLE{Franzmeier:141083,
      author       = {Franzmeier, Nicolai and Ren, Jinyi and Damm, Alexander and
                      Monté-Rubio, Gemma and Boada, Mercè and Ruiz, Agustín and
                      Ramirez, Alfredo and Jessen, Frank and Düzel, Emrah and
                      Rodríguez Gómez, Octavio and Benzinger, Tammie and Goate,
                      Alison and Karch, Celeste M and Fagan, Anne M and McDade,
                      Eric and Bürger, Katharina and Levin, Johannes and Duering,
                      Marco and Dichgans, Martin and Suárez-Calvet, Marc and
                      Haass, Christian and Gordon, Brian A and Lim, Yen Ying and
                      Masters, Colin L and Janowitz, Daniel and Catak, Cihan and
                      Wolfsgruber, Steffen and Wagner, Michael and Milz, Esther
                      and Moreno-Grau, Sonia and Teipel, Stefan and Grothe, Michel
                      J and Kilimann, Ingo and Rossor, Martin and Fox, Nick and
                      Laske, Christoph and Chhatwal, Jasmeer and Falkai, Peter and
                      Perneczky, Robert and Lee, Jae-Hong and Spottke, Annika and
                      Boecker, Henning and Brosseron, Frederic and Fließbach,
                      Klaus and Heneka, Michael T and Nestor, Peter and Peters,
                      Oliver and Fuentes Casan, Manuel and Menne, Felix and
                      Priller, Josef and Spruth, Eike J and Franke, Christiana and
                      Schneider, Anja and Westerteicher, Christine and Speck,
                      Oliver and Wiltfang, Jens and Bartels, Claudia and Araque
                      Caballero, Miguel Ángel and Metzger, Coraline and Bittner,
                      Daniel and Salloway, Stephen and Danek, Adrian and
                      Hassenstab, Jason and Yakushev, Igor and Schofield, Peter R
                      and Morris, John C and Bateman, Randall J and Ewers,
                      Michael},
      title        = {{T}he {BDNFV}al66{M}et {SNP} modulates the association
                      between beta-amyloid and hippocampal disconnection in
                      {A}lzheimer's disease.},
      journal      = {Molecular psychiatry},
      volume       = {26},
      number       = {2},
      issn         = {1359-4184},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {DZNE-2020-07405},
      pages        = {614-628},
      year         = {2021},
      abstract     = {In Alzheimer's disease (AD), a single-nucleotide
                      polymorphism in the gene encoding brain-derived neurotrophic
                      factor (BDNFVal66Met) is associated with worse impact of
                      primary AD pathology (beta-amyloid, Aβ) on
                      neurodegeneration and cognitive decline, rendering
                      BDNFVal66Met an important modulating factor of cognitive
                      impairment in AD. However, the effect of BDNFVal66Met on
                      functional networks that may underlie cognitive impairment
                      in AD is poorly understood. Using a cross-validation
                      approach, we first explored in subjects with autosomal
                      dominant AD (ADAD) from the Dominantly Inherited Alzheimer
                      Network (DIAN) the effect of BDNFVal66Met on resting-state
                      fMRI assessed functional networks. In seed-based
                      connectivity analysis of six major large-scale networks, we
                      found a stronger decrease of hippocampus (seed) to
                      medial-frontal connectivity in the BDNFVal66Met carriers
                      compared to BDNFVal homozogytes. BDNFVal66Met was not
                      associated with connectivity in any other networks. Next, we
                      tested whether the finding of more pronounced decrease in
                      hippocampal-medial-frontal connectivity in BDNFVal66Met
                      could be also found in elderly subjects with sporadically
                      occurring Aβ, including a group with subjective cognitive
                      decline (N = 149, FACEHBI study) and a group ranging
                      from preclinical to AD dementia (N = 114, DELCODE
                      study). In both of these independently recruited groups,
                      BDNFVal66Met was associated with a stronger effect of more
                      abnormal Aβ-levels (assessed by biofluid-assay or
                      amyloid-PET) on hippocampal-medial-frontal connectivity
                      decreases, controlled for hippocampus volume and other
                      confounds. Lower hippocampal-medial-frontal connectivity was
                      associated with lower global cognitive performance in the
                      DIAN and DELCODE studies. Together these results suggest
                      that BDNFVal66Met is selectively associated with a higher
                      vulnerability of hippocampus-frontal connectivity to primary
                      AD pathology, resulting in greater AD-related cognitive
                      impairment.},
      cin          = {AG Jessen / AG Düzel / AG Höglinger 1 / AG Levin / AG
                      Haass / AG Wagner / AG Teipel / AG Jucker / Patient Studies
                      Bonn / AG Boecker / AG Heneka ; AG Heneka / AG Nestor / AG
                      Endres / Clinical Dementia Research Bonn / AG Wiltfang / AG
                      Müller / Delcode},
      ddc          = {610},
      cid          = {I:(DE-2719)1011102 / I:(DE-2719)5000006 /
                      I:(DE-2719)1110002 / I:(DE-2719)1111016 / I:(DE-2719)1110007
                      / I:(DE-2719)1011201 / I:(DE-2719)1510100 /
                      I:(DE-2719)1210001 / I:(DE-2719)1011101 / I:(DE-2719)1011202
                      / I:(DE-2719)1011303 / I:(DE-2719)1310001 /
                      I:(DE-2719)1811005 / I:(DE-2719)1011305 / I:(DE-2719)1410006
                      / I:(DE-2719)1310003 / I:(DE-2719)5000034},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
                      - Clinical and Health Care Research (POF3-344) / 352 -
                      Disease Mechanisms (POF4-352) / 354 - Disease Prevention and
                      Healthy Aging (POF4-354) / 353 - Clinical and Health Care
                      Research (POF4-353)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344 /
                      G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-354 /
                      G:(DE-HGF)POF4-353},
      experiment   = {EXP:(DE-2719)DELCODE-20140101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30899092},
      pmc          = {pmc:PMC6754794},
      doi          = {10.1038/s41380-019-0404-6},
      url          = {https://pub.dzne.de/record/141083},
}