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@ARTICLE{Lohmann:163453,
      author       = {Lohmann, Stephanie and Grigoletto, Jessica and Bernis,
                      Maria Eugenia and Pesch, Verena and Ma, Liang and Reithofer,
                      Sara and Tamgüney, Gültekin},
      title        = {{I}schemic stroke causes {P}arkinson's disease-like
                      pathology and symptoms in transgenic mice overexpressing
                      alpha-synuclein.},
      journal      = {Acta Neuropathologica Communications},
      volume       = {10},
      number       = {1},
      issn         = {2051-5960},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DZNE-2022-00213},
      pages        = {26},
      year         = {2022},
      abstract     = {The etiology of Parkinson's disease is poorly understood
                      and is most commonly associated with advancing age, genetic
                      predisposition, or environmental toxins. Epidemiological
                      findings suggest that patients have a higher risk of
                      developing Parkinson's disease after ischemic stroke, but
                      this potential causality lacks mechanistic evidence. We
                      investigated the long-term effects of ischemic stroke on
                      pathogenesis in hemizygous TgM83 mice, which express human
                      α-synuclein with the familial A53T mutation without
                      developing any neuropathology or signs of neurologic disease
                      for more than 600 days. We induced transient focal ischemia
                      by middle cerebral artery occlusion in 2-month-old TgM83+/-
                      mice and monitored their behavior and health status for up
                      to 360 days post surgery. Groups of mice were sacrificed at
                      14, 30, 90, 180, and 360 days after surgery for
                      neuropathological analysis of their brains. Motor deficits
                      first appeared 6 months after focal ischemia and worsened
                      until 12 months afterward. Immunohistochemical analysis
                      revealed ischemia-induced neuronal loss in the infarct
                      region and astrogliosis and microgliosis indicative of an
                      inflammatory response, which was most pronounced at 14 days
                      post surgery. Infarct volume and inflammation gradually
                      decreased in size and severity until 180 days post surgery.
                      Surprisingly, neuronal loss and inflammation were increased
                      again by 360 days post surgery. These changes were
                      accompanied by a continuous increase in α-synuclein
                      aggregation, its neuronal deposition, and a late loss of
                      dopaminergic neurons in the substantia nigra, which we
                      detected at 360 days post surgery. Control animals that
                      underwent sham surgery without middle cerebral artery
                      occlusion showed no signs of disease or neuropathology. Our
                      results establish a mechanistic link between ischemic stroke
                      and Parkinson's disease and provide an animal model for
                      studying possible interventions.},
      keywords     = {Animals / Disease Models, Animal / Dopaminergic Neurons:
                      pathology / Humans / Infarction, Middle Cerebral Artery:
                      complications / Inflammation: complications / Ischemic
                      Stroke / Mice / Mice, Transgenic / Parkinson Disease:
                      complications / Parkinson Disease: genetics / Parkinson
                      Disease: pathology / alpha-Synuclein: genetics /
                      Alpha-synuclein (Other) / Ischemia (Other) / Ischemic stroke
                      (Other) / Parkinson’s disease (Other) / Stroke (Other) /
                      Synucleinopathy (Other)},
      cin          = {AG Vorberg / AG Tamgüney 2 / AG Capasso},
      ddc          = {610},
      cid          = {I:(DE-2719)1013004 / I:(DE-2719)1013022 /
                      I:(DE-2719)1013033},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 351 - Brain Function
                      (POF4-351)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35209932},
      pmc          = {pmc:PMC8867857},
      doi          = {10.1186/s40478-022-01327-6},
      url          = {https://pub.dzne.de/record/163453},
}