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@ARTICLE{Walberer:185743,
      author       = {Walberer, M. and Jantzen, S. U. and Backes, H. and Rueger,
                      M. A. and Keuters, M. H. and Neumaier, B. and Hoehn, M. and
                      Fink, Gereon Rudolf and Graf, R. and Schroeter, M.},
      title        = {{I}n-vivo detection of inflammation and neurodegeneration
                      in the chronic phase after permanent embolic stroke in rats},
      journal      = {Brain research},
      volume       = {1581},
      issn         = {0006-8993},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {FZJ-2014-07168},
      pages        = {80-88},
      year         = {2014},
      abstract     = {Neuroinflammation with microglia activation (MA)
                      constitutes a key tissue response in acute stroke. Until
                      now, its course in the chronic stage is less well defined.
                      Here, we investigated (i) neuroinflammation in the chronic
                      stage of a rat model of embolic stroke (n=6), and (ii)
                      whether this process can be visualized in vivo by multimodal
                      imaging using Magnetic Resonance Imaging (MRI) and
                      Positron-Emission-Tomography (PET). Imaging data were
                      verified using histology and immunohistochemistry.
                      Repetitive PET studies until week 6 after stroke reveal
                      poststroke inflammation as a dynamic process that involved
                      the infarct, the surrounding tissue and secondary
                      degenerating areas in a complex fashion. At the end, 7
                      months after stroke, neuroinflammation had almost completely
                      vanished at the lesion side. In contrast, remote from the
                      primarily infarcted areas, a marked T2⁎- hypointensity was
                      detected in the ipsilateral thalamus. In the corresponding
                      area, [11C]PK11195-PET detected microglia activation.
                      Immunohistochemistry confirmed activated microglia in the
                      ipsilateral thalamus with signs of extensive phagocytosis
                      and iron deposition around plaque-like amyloid deposition.
                      Neuronal staining (NeuN) revealed pronounced neuronal loss
                      as an endpoint of neurodegeneration in these areas.In
                      conclusion, the data demonstrate not only ongoing thalamic
                      neuroinflammation but also marked neurodegeneration remote
                      from the lesion site in the chronic phase after stroke in
                      rats. Both, neuroinflammation and neurodegeneration were
                      accessible to (immuno-) histochemical methods as well as to
                      in vivo methods using [11C]PK11195-PET and T2⁎-weighted
                      MRI. Although the functional roles of these dynamic
                      processes remain to be elucidated, ongoing destruction of
                      neuronal tissue is conceivable. Its inhibition using
                      anti-inflammatory substances may be beneficial in chronic
                      post-stroke conditions, while multimodal imaging can be used
                      to evaluate putative therapeutic effects in vivo.},
      cin          = {INM-3},
      ddc          = {150},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {333 - Pathophysiological Mechanisms of Neurological and
                      Psychiatric Diseases (POF2-333) / 89572 - (Dys-)function and
                      Plasticity (POF2-89572)},
      pid          = {G:(DE-HGF)POF2-333 / G:(DE-HGF)POF2-89572},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000342542100008},
      doi          = {10.1016/j.brainres.2014.05.030},
      url          = {https://juser.fz-juelich.de/record/185743},
}