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@ARTICLE{Nabbi:848313,
      author       = {Nabbi, Danje and Elmenhorst, David and Oskamp, Angela and
                      Laskowski, Stefanie and Bauer, Andreas and Kroll, Tina},
      title        = {{E}ffects of {L}ong-{T}erm {C}affeine {C}onsumption on the
                      {A}denosine {A}1 {R}eceptor in the {R}at {B}rain: an {I}n
                      {V}ivo {PET} {S}tudy with [18{F}]{CPFPX}},
      journal      = {Molecular imaging $\&$ biology},
      volume       = {20},
      number       = {2},
      issn         = {1860-2002},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2018-03558},
      pages        = {284 - 291},
      year         = {2018},
      abstract     = {Purpose- Caffeine, a nonselective antagonist of adenosine
                      receptors, is the most popular psychostimulant worldwide.
                      Recently, a protective role of moderate chronic caffeine
                      consumption against neurodegenerative diseases such as
                      Alzheimer’s and Parkinson’s disease has been discussed.
                      Thus, aim of the present study was an in vivo investigation
                      of effects of long-term caffeine consumption on the
                      adenosine A1 receptor (A1AR) in the rat
                      brain.ProceduresSixteen adult, male rats underwent five
                      positron emission tomography (PET) scans with the highly
                      selective A1AR radioligand [18F]CPFPX in order to determine
                      A1AR availability. After the first baseline PET scan, the
                      animals were assigned to two groups: Caffeine treatment and
                      control group. The caffeine-treated animals received
                      caffeinated tap water (30 mg/kg bodyweight/day,
                      corresponding to 4–5 cups of coffee per day in humans) for
                      12 weeks. Subsequently, caffeine was withdrawn and repeated
                      PET measurements were performed on day 1, 2, 4, and 7 of
                      caffeine withdrawal. The control animals were measured
                      according to the same time schedule.ResultsAt day 1, after
                      4.4 h of caffeine withdrawal, a significant decrease (−
                      $34.5\%,$ p < 0.001) of whole brain A1AR availability was
                      observed. Unlike all other investigated brain regions in
                      caffeine-treated rats, the hypothalamus and nucleus
                      accumbens showed no significant intraindividual differences
                      between baseline and first withdrawal PET scan. After
                      approximately 27 h of caffeine withdrawal, the region- and
                      group-specific effects disappeared and A1AR availability
                      settled around baseline.ConclusionsThe present study
                      provides evidence that chronic caffeine consumption does not
                      lead to persistent changes in functional availability of
                      cerebral A1ARs which have previously been associated with
                      neuroprotective effects of caffeine. The acute and
                      region-specific decrease in cerebral A1AR availability
                      directly after caffeine withdrawal is most likely caused by
                      residual amounts of caffeine metabolites disguising an
                      unchanged A1AR expression at this early time-point.},
      cin          = {INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28895043},
      UT           = {WOS:000428064400015},
      doi          = {10.1007/s11307-017-1116-4},
      url          = {https://juser.fz-juelich.de/record/848313},
}