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@ARTICLE{Backes:280871,
      author       = {Backes, Heiko and Walberer, Maureen and Ladwig, Anne and
                      Rueger, Maria A. and Neumaier, Bernd and Endepols, Heike and
                      Hoehn, Mathias and Fink, Gereon R. and Schroeter, Michael
                      and Graf, Rudolf},
      title        = {{G}lucose consumption of inflammatory cells masks metabolic
                      deficits in the brain},
      journal      = {NeuroImage},
      volume       = {128},
      issn         = {1053-8119},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {FZJ-2016-00582},
      pages        = {54 - 62},
      year         = {2016},
      abstract     = {Inflammatory cells such as microglia need energy to exert
                      their functions and to maintain their cellular integrity and
                      membrane potential. Subsequent to cerebral ischemia,
                      inflammatory cells infiltrate tissue with limited blood flow
                      where neurons and astrocytes died due to insufficient supply
                      with oxygen and glucose. Using dual tracer positron emission
                      tomography (PET), we found that concomitant with the
                      presence of inflammatory cells, transport and consumption of
                      glucose increased up to normal levels but returned to
                      pathological levels as soon as inflammatory cells
                      disappeared. Thus, inflammatory cells established sufficient
                      glucose supply to satisfy their energy demands even in
                      regions with insufficient supply for neurons and astrocytes
                      to survive. Our data suggest that neurons and astrocytes
                      died from oxygen deficiency and inflammatory cells
                      metabolized glucose non-oxidatively in regions with residual
                      availability. As a consequence, glucose metabolism of
                      inflammatory cells can mask metabolic deficits in
                      neurodegenerative diseases. We further found that the PET
                      tracer did not bind to inflammatory cells in severely
                      hypoperfused regions and thus only a part of the
                      inflammation was detected. We conclude that glucose
                      consumption of inflammatory cells should be taken into
                      account when analyzing disease-related alterations of local
                      cerebral metabolism.},
      cin          = {INM-3 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000370386000006},
      pubmed       = {pmid:26747749},
      doi          = {10.1016/j.neuroimage.2015.12.044},
      url          = {https://juser.fz-juelich.de/record/280871},
}