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@ARTICLE{EkmarkLewn:259712,
      author       = {Ekmark-Lewén, S. and Aniszewska, A. and Molisak, A. and
                      Gumucio, A. and Lindström, V. and Kahle, P. J. and
                      Nordström, E. and Möller, C. and Fälting, J. and
                      Lannfelt, L. and Bergström, J. and Ingelsson, M.},
      title        = {{R}eduction of brain stem pathology and transient
                      amelioration of early cognitive symptoms in transgenic mice
                      treated with a monoclonal antibody against α-synuclein
                      oligomers/protofibrils.},
      journal      = {Aging brain},
      volume       = {4},
      issn         = {2589-9589},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DZNE-2023-00784},
      pages        = {100086},
      year         = {2023},
      abstract     = {Immunotherapy against alpha-synuclein (α-syn) is a
                      promising novel treatment strategy for Parkinson's disease
                      (PD) and related α-synucleinopathies. We have previously
                      shown that systemic treatment with the monoclonal
                      oligomer/protofibril-selective antibody mAb47 targeting
                      cytotoxic α-syn leads to reduced central nervous system
                      levels of such species as well as an indication of reduced
                      late-stage symptoms in aged (Thy-1)-h[A30P] α-syn
                      transgenic mice. Here, we performed an early-onset long-term
                      treatment study with this antibody to evaluate effects on
                      brain pathology and behavioral outcomes in the same mouse
                      model. Compared to the placebo group, the treatment strongly
                      reduced phosphorylated α-syn (pS129 α-syn) pathology in
                      the upper brain stem. Moreover, a preserved recognition
                      memory and risk assessment behavior could be seen in
                      antibody-treated mice at six months of age, even although
                      these effects were no longer significant at eleven months of
                      age. Importantly, no evidence of inflammatory responses or
                      other potential toxic effects was seen with the treatment.
                      Taken together, this study supports the strategy to target
                      α-syn oligomers/protofibrils with monoclonal antibodies to
                      counteract early symptoms and slow down the progression of
                      PD and other α-synucleinopathies.},
      keywords     = {Alpha-synuclein transgenic mice (Other) / Behavioral
                      outcome (Other) / Immunotherapy (Other) /
                      Oligomer/protofibril-selective antibody (Other) / Oligomers
                      (Other)},
      cin          = {AG Kahle},
      ddc          = {610},
      cid          = {I:(DE-2719)1210000-4},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37559953},
      pmc          = {pmc:PMC10407822},
      doi          = {10.1016/j.nbas.2023.100086},
      url          = {https://pub.dzne.de/record/259712},
}