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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},
}