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@ARTICLE{Catterson:292292,
      author       = {J. H. Catterson and E. N. Mouofo and I. López De Toledo
                      Soler and G. Lean and S. Dlamini and P. Liddell and G. Voong
                      and T. Katsinelos$^*$ and Y.-C. Wang and N. Schoovaerts and
                      P. Verstreken and T. L. Spires-Jones and C. S. Durrant},
      title        = {{D}rosophila appear resistant to trans-synaptic tau
                      propagation.},
      journal      = {Brain communications},
      volume       = {6},
      number       = {4},
      issn         = {2632-1297},
      address      = {[Großbritannien]},
      publisher    = {Guarantors of Brain},
      reportid     = {DKFZ-2024-01653},
      pages        = {fcae256},
      year         = {2024},
      abstract     = {Alzheimer's disease is the most common cause of dementia in
                      the elderly, prompting extensive efforts to pinpoint novel
                      therapeutic targets for effective intervention. Among the
                      hallmark features of Alzheimer's disease is the development
                      of neurofibrillary tangles comprised of hyperphosphorylated
                      tau protein, whose progressive spread throughout the brain
                      is associated with neuronal death. Trans-synaptic
                      propagation of tau has been observed in mouse models, and
                      indirect evidence for tau spread via synapses has been
                      observed in human Alzheimer's disease. Halting tau
                      propagation is a promising therapeutic target for
                      Alzheimer's disease; thus, a scalable model system to screen
                      for modifiers of tau spread would be very useful for the
                      field. To this end, we sought to emulate the trans-synaptic
                      spread of human tau in Drosophila melanogaster. Employing
                      the trans-Tango circuit mapping technique, we investigated
                      whether tau spreads between synaptically connected neurons.
                      Immunohistochemistry and confocal imaging were used to look
                      for tau propagation. Examination of hundreds of flies
                      expressing four different human tau constructs in two
                      distinct neuronal populations reveals a robust resistance in
                      Drosophila to the trans-synaptic spread of human tau. This
                      resistance persisted in lines with concurrent expression of
                      amyloid-β, in lines with global human tau knock-in to
                      provide a template for human tau in downstream neurons, and
                      with manipulations of temperature. These negative data are
                      important for the field as we establish that Drosophila
                      expressing human tau in subsets of neurons are unlikely to
                      be useful to perform screens to find mechanisms to reduce
                      the trans-synaptic spread of tau. The inherent resistance
                      observed in Drosophila may serve as a valuable clue,
                      offering insights into strategies for impeding tau spread in
                      future studies.},
      keywords     = {Alzheimer’s disease (Other) / Drosophila melanogaster
                      (Other) / neurodegeneration (Other) / tau (Other) /
                      trans-synaptic (Other)},
      cin          = {B180},
      ddc          = {610},
      cid          = {I:(DE-He78)B180-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39130515},
      pmc          = {pmc:PMC11316205},
      doi          = {10.1093/braincomms/fcae256},
      url          = {https://inrepo02.dkfz.de/record/292292},
}