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@ARTICLE{Davies:259960,
      author       = {Davies, Caitlin and Tulloch, Jane and Yip, Ellie and
                      Currie, Lydia and Colom-Cadena, Marti and Wegmann, Susanne
                      and Hyman, Bradley T and Wilkins, Lewis and Hooley, Monique
                      and Tzioras, Makis and Spires-Jones, Tara L},
      title        = {{A}polipoprotein {E} isoform does not influence
                      trans-synaptic spread of tau pathology in a mouse model.},
      journal      = {Brain and neuroscience advances},
      volume       = {7},
      issn         = {2398-2128},
      address      = {Thousand Oaks, CA},
      publisher    = {Sage Publishing},
      reportid     = {DZNE-2023-00813},
      pages        = {23982128231191046},
      year         = {2023},
      abstract     = {A key hallmark of Alzheimer's disease (AD) is the
                      accumulation of hyperphosphorylated tau in neurofibrillary
                      tangles. This occurs alongside neuroinflammation and
                      neurodegeneration. Pathological tau propagates through the
                      AD brain in a defined manner, which correlates with neuron
                      and synapse loss and cognitive decline. One proposed
                      mechanism of tau spread is through synaptically connected
                      brain structures. Apolipoprotein E4 (APOE4) genotype is the
                      strongest genetic risk factor for late-onset AD and is
                      associated with increased tau burden. Whether the
                      apolipoprotein E (APOE) genotype influences
                      neurodegeneration via tau spread is currently unknown. Here,
                      we demonstrate that virally expressed human tau (with the
                      P301L mutation) injected into mouse entorhinal cortex at 5-6
                      months or 15-16 months of age spreads trans-synaptically to
                      the hippocampus by 14 weeks post-injection. Injections of
                      tau in mice expressing human APOE2, APOE3 or APOE4, as well
                      as APOE knock-outs, showed that tau can spread
                      trans-synaptically in all genotypes and that APOE genotype
                      and age do not affect the spread of tau. These data suggest
                      that APOE genotype is not directly linked to synaptic spread
                      of tau in our model, but other mechanisms involving non-cell
                      autonomous manners of tau spread are still possible.},
      keywords     = {Alzheimer (Other) / apolipoprotein E (Other) / array
                      tomography (Other) / synapse (Other) / tau (Other) /
                      tauopathy (Other)},
      cin          = {AG Wegmann},
      ddc          = {610},
      cid          = {I:(DE-2719)1810006},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37600228},
      pmc          = {pmc:PMC10433884},
      doi          = {10.1177/23982128231191046},
      url          = {https://pub.dzne.de/record/259960},
}