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@ARTICLE{Leiter:163270,
      author       = {Leiter, Odette and Zhuo, Zhan and Rust, Ruslan and
                      Wasielewska, Joanna M and Grönnert, Lisa and Kowal, Susann
                      and Overall, Rupert W and Adusumilli, Vijay S and Blackmore,
                      Daniel G and Southon, Adam and Ganio, Katherine and
                      McDevitt, Christopher A and Rund, Nicole and Brici, David
                      and Mudiyan, Imesh Aththanayake and Sykes, Alexander M and
                      Rünker, Annette E and Zocher, Sara and Ayton, Scott and
                      Bush, Ashley I and Bartlett, Perry F and Hou, Sheng-Tao and
                      Kempermann, Gerd and Walker, Tara L},
      title        = {{S}elenium mediates exercise-induced adult neurogenesis and
                      reverses learning deficits induced by hippocampal injury and
                      aging.},
      journal      = {Cell metabolism},
      volume       = {34},
      number       = {3},
      issn         = {1550-4131},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DZNE-2022-00050},
      pages        = {408 - 423.e8},
      year         = {2022},
      note         = {(CC BY-NC-ND)},
      abstract     = {Although the neurogenesis-enhancing effects of exercise
                      have been extensively studied, the molecular mechanisms
                      underlying this response remain unclear. Here, we propose
                      that this is mediated by the exercise-induced systemic
                      release of the antioxidant selenium transport protein,
                      selenoprotein P (SEPP1). Using knockout mouse models, we
                      confirmed that SEPP1 and its receptor low-density
                      lipoprotein receptor-related protein 8 (LRP8) are required
                      for the exercise-induced increase in adult hippocampal
                      neurogenesis. In vivo selenium infusion increased
                      hippocampal neural precursor cell (NPC) proliferation and
                      adult neurogenesis. Mimicking the effect of exercise through
                      dietary selenium supplementation restored neurogenesis and
                      reversed the cognitive decline associated with aging and
                      hippocampal injury, suggesting potential therapeutic
                      relevance. These results provide a molecular mechanism
                      linking exercise-induced changes in the systemic environment
                      to the activation of quiescent hippocampal NPCs and their
                      subsequent recruitment into the neurogenic trajectory.},
      keywords     = {Aging / Animals / Cell Proliferation / Hippocampus / Mice /
                      Neural Stem Cells: metabolism / Neurogenesis: physiology /
                      Selenium: metabolism / Selenium: pharmacology / adult
                      neurogenesis (Other) / aging (Other) / dentate gyrus (Other)
                      / endothelin-1 (Other) / exercise (Other) / hippocampal
                      lesion (Other) / hippocampus (Other) / neural precursor cell
                      (Other) / neural stem cell (Other) / selenium (Other)},
      cin          = {Dresden common / AG Kempermann / AG Toda},
      ddc          = {570},
      cid          = {I:(DE-2719)6000013 / I:(DE-2719)1710001 /
                      I:(DE-2719)1710014},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35120590},
      doi          = {10.1016/j.cmet.2022.01.005},
      url          = {https://pub.dzne.de/record/163270},
}