% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Bedrosian:155271,
      author       = {Bedrosian, Tracy A and Houtman, Judith and Eguiguren, Juan
                      Sebastian and Ghassemzadeh, Saeed and Rund, Nicole and
                      Novaresi, Nicole M and Hu, Lauren and Parylak, Sarah L. and
                      Denli, Ahmet M and Randolph-Moore, Lynne and Namba, Takashi
                      and Gage, Fred H and Toda, Tomohisa},
      title        = {{L}amin {B}1 decline underlies age‐related loss of adult
                      hippocampal neurogenesis},
      journal      = {The EMBO journal},
      volume       = {40},
      number       = {3},
      issn         = {1460-2075},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2021-00551},
      pages        = {e105819},
      year         = {2021},
      abstract     = {Neurogenesis in the adult hippocampus declines with age, a
                      process that has been implicated in cognitive and emotional
                      impairments. However, the mechanisms underlying this decline
                      have remained elusive. Here, we show that the age-dependent
                      downregulation of lamin B1, one of the nuclear lamins in
                      adult neural stem/progenitor cells (ANSPCs), underlies
                      age-related alterations in adult hippocampal neurogenesis.
                      Our results indicate that higher levels of lamin B1 in
                      ANSPCs safeguard against premature differentiation and
                      regulate the maintenance of ANSPCs. However, the level of
                      lamin B1 in ANSPCs declines during aging. Precocious loss of
                      lamin B1 in ANSPCs transiently promotes neurogenesis but
                      eventually depletes it. Furthermore, the reduction of lamin
                      B1 in ANSPCs recapitulates age-related anxiety-like behavior
                      in mice. Our results indicate that the decline in lamin B1
                      underlies stem cell aging and impacts the homeostasis of
                      adult neurogenesis and mood regulation.},
      keywords     = {Aging: genetics / Aging: metabolism / Animals / Anxiety:
                      genetics / Cell Differentiation / Cell Line / Disease
                      Models, Animal / Down-Regulation / Female / Hippocampus:
                      cytology / Hippocampus: metabolism / Lamin Type B: genetics
                      / Lamin Type B: metabolism / Male / Mice / Neural Stem
                      Cells: cytology / Neural Stem Cells: metabolism /
                      Neurogenesis / Rats},
      cin          = {AG Toda},
      ddc          = {570},
      cid          = {I:(DE-2719)1710014},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33300615},
      pubmed       = {33300615},
      pmc          = {pmc:PMC7849303},
      doi          = {10.15252/embj.2020105819},
      url          = {https://pub.dzne.de/record/155271},
}