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@ARTICLE{Neuner:137269,
      author       = {Neuner, Johanna and Filser, Severin and Michalakis,
                      Stylianos and Biel, Martin and Herms, Jochen},
      title        = {{A}30{P} α-{S}ynuclein interferes with the stable
                      integration of adult-born neurons into the olfactory
                      network.},
      journal      = {Scientific reports},
      volume       = {4},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DZNE-2020-03591},
      pages        = {3931},
      year         = {2014},
      abstract     = {Impaired olfaction is an early symptom in Parkinson disease
                      (PD), although the exact cause is as yet unknown. Here, we
                      investigated the link between PD-related mutant α-Synuclein
                      (α-SYN) pathology and olfactory deficit, by examining the
                      integration of adult-born neurons in the olfactory bulb (OB)
                      of A30P α-SYN overexpressing mice. To this end, we chose to
                      label one well-known vulnerable subpopulation of adult-born
                      cells, the dopaminergic neurons. Using in vivo two-photon
                      imaging, we followed the dynamic process of neuronal
                      turnover in transgenic A30P α-SYN and wild-type mice over a
                      period of 2.5 months. Our results reveal no difference in
                      the number of cells that reach, and possibly integrate into,
                      the glomerular layer in the OB. However, in mutant
                      transgenic mice these new neurons have a significantly
                      shortened survival, resulting in an overall reduction in the
                      addition of neurons to the glomerular layer over time. We
                      therefore propose unstable integration and impaired
                      homeostasis of functional new neurons as a likely
                      contributor to odour discrimination deficits in mutant
                      α-SYN mice.},
      keywords     = {Animals / Dopamine: biosynthesis / Dopaminergic Neurons:
                      diagnostic imaging / Lentivirus: genetics / Mice / Mice,
                      Inbred C57BL / Mice, Transgenic / Olfaction Disorders:
                      genetics / Olfactory Bulb: physiopathology / Parkinson
                      Disease: diagnosis / Parkinson Disease: genetics / Protein
                      Aggregation, Pathological: metabolism / Radiography / Smell:
                      genetics / Smell: physiology / alpha-Synuclein: genetics /
                      SNCA protein, human (NLM Chemicals) / alpha-Synuclein (NLM
                      Chemicals) / Dopamine (NLM Chemicals)},
      cin          = {Ext LMU / AG Herms},
      ddc          = {600},
      cid          = {I:(DE-2719)5000048 / I:(DE-2719)1110001},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24488133},
      pmc          = {pmc:PMC3909899},
      doi          = {10.1038/srep03931},
      url          = {https://pub.dzne.de/record/137269},
}