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@ARTICLE{Schroeder:276182,
      author       = {Schroeder, Sophie and Sakib, M Sadman and Krüger, Dennis
                      Manfred and Pena, Tonatiuh and Burkhardt, Susanne and
                      Schütz, Anna-Lena and Sananbenesi, Farahnaz and Fischer,
                      Andre},
      title        = {{L}nc{RNA} 3222401{L}13{R}ik {I}s {U}pregulated in {A}ging
                      {A}strocytes and {R}egulates {N}euronal {S}upport {F}unction
                      {T}hrough {I}nteraction with {N}pas3.},
      journal      = {Non-Coding RNA},
      volume       = {11},
      number       = {1},
      issn         = {2311-553X},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DZNE-2025-00250},
      pages        = {2},
      year         = {2025},
      abstract     = {Aging leads to cognitive decline and increased risk of
                      neurodegenerative diseases. While molecular changes in
                      central nervous system (CNS) cells contribute to this
                      decline, the mechanisms are not fully understood. Long
                      non-coding RNAs (lncRNAs) are key regulators of cellular
                      functions. Background/Objectives: The roles of lncRNAs in
                      aging, especially in glial cells, are not well
                      characterized. Methods: We investigated lncRNA expression in
                      non-neuronal cells from aged mice and identified
                      3222401L13Rik, a previously unstudied lncRNA, as upregulated
                      in astrocytes during aging. Results: Knockdown of
                      3222401L13Rik in primary astrocytes revealed its critical
                      role in regulating genes for neuronal support and synapse
                      organization, a function conserved in human iPSC-derived
                      astrocytes. A 3222401L13Rik interacts with the transcription
                      factor Neuronal PAS Domain Protein 3 (Npas3), and
                      overexpression of Npas3 rescues deficits in astrocytes
                      lacking 3222401L13Rik. Conclusions: These data suggest that
                      3222401L13Rik upregulation may help delay age-related
                      cognitive decline.},
      keywords     = {Alzheimer’s disease (Other) / aging (Other) / astrocytes
                      (Other) / brain (Other) / lncRNA (Other) / neurodegenerative
                      diseases (Other) / non-coding RNA (Other) / transcriptomics
                      (Other)},
      cin          = {AG Fischer / Clinical Dementia Research (Göttingen) /
                      Bioinformatics Unit (Göttingen) / AG Sananbenesi},
      ddc          = {570},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)1440015 /
                      I:(DE-2719)1440016 / I:(DE-2719)1410004},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39846680},
      doi          = {10.3390/ncrna11010002},
      url          = {https://pub.dzne.de/record/276182},
}