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@ARTICLE{Schrder:271879,
      author       = {Schröder, Sophie and Fuchs, Ulrike and Gisa, Verena and
                      Pena, Tonatiuh and Krüger, Dennis M and Hempel, Nina and
                      Burkhardt, Susanne and Salinas, Gabriela and Schütz,
                      Anna-Lena and Delalle, Ivana and Sananbenesi, Farahnaz and
                      Fischer, Andre},
      title        = {{PRDM}16-{DT} is a novel lnc{RNA} that regulates astrocyte
                      function in {A}lzheimer's disease.},
      journal      = {Acta neuropathologica},
      volume       = {148},
      number       = {1},
      issn         = {0001-6322},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2024-01091},
      pages        = {32},
      year         = {2024},
      abstract     = {Astrocytes provide crucial support for neurons,
                      contributing to synaptogenesis, synaptic maintenance, and
                      neurotransmitter recycling. Under pathological conditions,
                      deregulation of astrocytes contributes to neurodegenerative
                      diseases such as Alzheimer's disease (AD). While most
                      research in this field has focused on protein-coding genes,
                      non-coding RNAs, particularly long non-coding RNAs
                      (lncRNAs), have emerged as significant regulatory molecules.
                      In this study, we identified the lncRNA PRDM16-DT as highly
                      enriched in the human brain, where it is almost exclusively
                      expressed in astrocytes. PRDM16-DT and its murine homolog,
                      Prdm16os, are downregulated in the brains of AD patients and
                      in AD models. In line with this, knockdown of PRDM16-DT and
                      Prdm16os revealed its critical role in maintaining astrocyte
                      homeostasis and supporting neuronal function by regulating
                      genes essential for glutamate uptake, lactate release, and
                      neuronal spine density through interactions with the
                      RE1-Silencing Transcription factor (Rest) and Polycomb
                      Repressive Complex 2 (PRC2). Notably, CRISPR-mediated
                      overexpression of Prdm16os mitigated functional deficits in
                      astrocytes induced by stimuli linked to AD pathogenesis.
                      These findings underscore the importance of PRDM16-DT in
                      astrocyte function and its potential as a novel therapeutic
                      target for neurodegenerative disorders characterized by
                      astrocyte dysfunction.},
      keywords     = {Astrocytes: metabolism / Astrocytes: pathology / Alzheimer
                      Disease: genetics / Alzheimer Disease: metabolism /
                      Alzheimer Disease: pathology / RNA, Long Noncoding: genetics
                      / RNA, Long Noncoding: metabolism / Animals / Humans / Mice
                      / DNA-Binding Proteins: genetics / DNA-Binding Proteins:
                      metabolism / Transcription Factors: genetics / Transcription
                      Factors: metabolism / Male / Brain: metabolism / Brain:
                      pathology / Neurons: metabolism / Neurons: pathology / Mice,
                      Inbred C57BL / Alzheimer’s disease (Other) / Astrocyte
                      (Other) / Brain (Other) / Long-non-coding RNA (Other) /
                      Postmortem human brain (Other) / RNA, Long Noncoding (NLM
                      Chemicals) / DNA-Binding Proteins (NLM Chemicals) /
                      Transcription Factors (NLM Chemicals) / PRDM16 protein,
                      human (NLM Chemicals) / Prdm16 protein, mouse (NLM
                      Chemicals)},
      cin          = {AG Fischer / AG Sananbenesi / Bioinformatics Unit
                      (Göttingen)},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)1410004 /
                      I:(DE-2719)1440016},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11362476},
      pubmed       = {pmid:39207536},
      doi          = {10.1007/s00401-024-02787-x},
      url          = {https://pub.dzne.de/record/271879},
}