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@ARTICLE{Jovasevic:268840,
      author       = {Jovasevic, Vladimir and Wood, Elizabeth M and Cicvaric, Ana
                      and Zhang, Hui and Petrovic, Zorica and Carboncino, Anna and
                      Parker, Kendra K and Bassett, Thomas E and Moltesen, Maria
                      and Yamawaki, Naoki and Login, Hande and Kalucka, Joanna and
                      Sananbenesi, Farahnaz and Zhang, Xusheng and Fischer, Andre
                      and Radulovic, Jelena},
      title        = {{F}ormation of memory assemblies through the {DNA}-sensing
                      {TLR}9 pathway.},
      journal      = {Nature},
      volume       = {628},
      number       = {8006},
      issn         = {0028-0836},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DZNE-2024-00344},
      pages        = {145 - 153},
      year         = {2024},
      abstract     = {As hippocampal neurons respond to diverse types of
                      information1, a subset assembles into microcircuits
                      representing a memory2. Those neurons typically undergo
                      energy-intensive molecular adaptations, occasionally
                      resulting in transient DNA damage3-5. Here we found discrete
                      clusters of excitatory hippocampal CA1 neurons with
                      persistent double-stranded DNA (dsDNA) breaks, nuclear
                      envelope ruptures and perinuclear release of histone and
                      dsDNA fragments hours after learning. Following these early
                      events, some neurons acquired an inflammatory phenotype
                      involving activation of TLR9 signalling and accumulation of
                      centrosomal DNA damage repair complexes6. Neuron-specific
                      knockdown of Tlr9 impaired memory while blunting contextual
                      fear conditioning-induced changes of gene expression in
                      specific clusters of excitatory CA1 neurons. Notably, TLR9
                      had an essential role in centrosome function, including DNA
                      damage repair, ciliogenesis and build-up of perineuronal
                      nets. We demonstrate a novel cascade of learning-induced
                      molecular events in discrete neuronal clusters undergoing
                      dsDNA damage and TLR9-mediated repair, resulting in their
                      recruitment to memory circuits. With compromised TLR9
                      function, this fundamental memory mechanism becomes a
                      gateway to genomic instability and cognitive impairments
                      implicated in accelerated senescence, psychiatric disorders
                      and neurodegenerative disorders. Maintaining the integrity
                      of TLR9 inflammatory signalling thus emerges as a promising
                      preventive strategy for neurocognitive deficits.},
      keywords     = {Animals / Female / Male / Mice / Aging: genetics / Aging:
                      pathology / CA1 Region, Hippocampal: physiology /
                      Centrosome: metabolism / Cognitive Dysfunction: genetics /
                      Conditioning, Classical / DNA Breaks, Double-Stranded / DNA
                      Repair / Extracellular Matrix: metabolism / Fear / Genomic
                      Instability: genetics / Histones: metabolism / Inflammation:
                      genetics / Inflammation: immunology / Inflammation:
                      metabolism / Inflammation: pathology / Memory: physiology /
                      Mental Disorders: genetics / Neurodegenerative Diseases:
                      genetics / Neuroinflammatory Diseases: genetics / Neurons:
                      metabolism / Neurons: pathology / Nuclear Envelope:
                      pathology / Toll-Like Receptor 9: deficiency / Toll-Like
                      Receptor 9: genetics / Toll-Like Receptor 9: immunology /
                      Toll-Like Receptor 9: metabolism / Histones (NLM Chemicals)
                      / Tlr9 protein, mouse (NLM Chemicals) / Toll-Like Receptor 9
                      (NLM Chemicals)},
      cin          = {AG Sananbenesi / AG Fischer},
      ddc          = {500},
      cid          = {I:(DE-2719)1410004 / I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38538785},
      pmc          = {pmc:PMC10990941},
      doi          = {10.1038/s41586-024-07220-7},
      url          = {https://pub.dzne.de/record/268840},
}