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@ARTICLE{Bhattarai:145133,
      author       = {Bhattarai, Prabesh and Cosacak, Mehmet Ilyas and
                      Mashkaryan, Violeta and Demir, Sevgican and Popova,
                      Stanislava Dimitrova and Govindarajan, Nambirajan and
                      Brandt, Kerstin and Zhang, Yixin and Chang, Weipang and
                      Ampatzis, Konstantinos and Kizil, Caghan},
      title        = {{N}euron-glia interaction through {S}erotonin-{BDNF}-{NGFR}
                      axis enables regenerative neurogenesis in {A}lzheimer's
                      model of adult zebrafish brain.},
      journal      = {PLoS biology},
      volume       = {18},
      number       = {1},
      issn         = {1545-7885},
      address      = {Lawrence, KS},
      publisher    = {PLoS},
      reportid     = {DZNE-2020-00492},
      pages        = {e3000585},
      year         = {2020},
      abstract     = {It was recently suggested that supplying the brain with new
                      neurons could counteract Alzheimer's disease (AD). This
                      provocative idea requires further testing in experimental
                      models in which the molecular basis of disease-induced
                      neuronal regeneration could be investigated. We previously
                      found that zebrafish stimulates neural stem cell (NSC)
                      plasticity and neurogenesis in AD and could help to
                      understand the mechanisms to be harnessed for developing new
                      neurons in diseased mammalian brains. Here, by performing
                      single-cell transcriptomics, we found that amyloid
                      toxicity-induced interleukin-4 (IL4) promotes NSC
                      proliferation and neurogenesis by suppressing the tryptophan
                      metabolism and reducing the production of serotonin. NSC
                      proliferation was suppressed by serotonin via
                      down-regulation of brain-derived neurotrophic factor
                      (BDNF)-expression in serotonin-responsive periventricular
                      neurons. BDNF enhances NSC plasticity and neurogenesis via
                      nerve growth factor receptor A (NGFRA)/ nuclear factor
                      'kappa-light-chain-enhancer' of activated B-cells (NFkB)
                      signaling in zebrafish but not in rodents. Collectively, our
                      results suggest a complex neuron-glia interaction that
                      regulates regenerative neurogenesis after AD conditions in
                      zebrafish.},
      keywords     = {Age Factors / Alzheimer Disease: genetics / Alzheimer
                      Disease: pathology / Alzheimer Disease: physiopathology /
                      Animals / Animals, Genetically Modified / Brain: metabolism
                      / Brain: physiology / Brain-Derived Neurotrophic Factor:
                      genetics / Brain-Derived Neurotrophic Factor: metabolism /
                      Cell Communication: physiology / Disease Models, Animal /
                      Male / Mice / Mice, Transgenic / Nerve Regeneration:
                      genetics / Nerve Regeneration: physiology / Neural Stem
                      Cells: pathology / Neural Stem Cells: physiology /
                      Neurogenesis: physiology / Neuroglia: physiology /
                      Neuroimmunomodulation: physiology / Neuronal Plasticity:
                      physiology / Neurons: physiology / Receptors, Nerve Growth
                      Factor: genetics / Receptors, Nerve Growth Factor:
                      metabolism / Serotonin: genetics / Serotonin: metabolism /
                      Signal Transduction: genetics / Zebrafish / Zebrafish
                      Proteins: genetics / Zebrafish Proteins: metabolism /
                      Brain-Derived Neurotrophic Factor (NLM Chemicals) /
                      Receptors, Nerve Growth Factor (NLM Chemicals) / Zebrafish
                      Proteins (NLM Chemicals) / Serotonin (NLM Chemicals)},
      cin          = {AG Kizil / AG Kempermann 1 / Dresden Pre 2020 / AG Fischer
                      1},
      ddc          = {610},
      cid          = {I:(DE-2719)1710007 / I:(DE-2719)1710001 /
                      I:(DE-2719)6000013 / I:(DE-2719)1410002},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31905199},
      pmc          = {pmc:PMC6964913},
      doi          = {10.1371/journal.pbio.3000585},
      url          = {https://pub.dzne.de/record/145133},
}