% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Lin:1030414,
      author       = {Lin, Yu-Shiuan and Lange, Denise and Baur, Diego Manuel and
                      Foerges, Anna and Chu, Congying and Li, Changhong and
                      Elmenhorst, Eva-Maria and Neumaier, Bernd and Bauer, Andreas
                      and Aeschbach, Daniel and Landolt, Hans-Peter and
                      Elmenhorst, David},
      title        = {{R}epeated caffeine intake suppresses cerebral grey matter
                      responses to chronic sleep restriction in an {A}1 adenosine
                      receptor-dependent manner: a double-blind randomized
                      controlled study with {PET}-{MRI}},
      journal      = {Scientific reports},
      volume       = {14},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {FZJ-2024-05287},
      pages        = {12724},
      year         = {2024},
      note         = {This work was supported by the Institute for Scientific
                      Information on Coffee (ISIC), the Swiss National
                      ScienceFoundation, the Clinical Research Priority Program
                      Sleep $\&$ Health of the University of Zurich, the
                      AeronauticsProgram of the German Aerospace Center, and
                      respective institutional funds from all contributing
                      institutions},
      abstract     = {Evidence has shown that both sleep loss and daily caffeine
                      intake can induce changes in greymatter (GM). Caffeine is
                      frequently used to combat sleepiness and impaired
                      performance caused byinsufficient sleep. It is unclear (1)
                      whether daily use of caffeine could prevent or exacerbate
                      the GMalterations induced by 5‑day sleep restriction (i.e.
                      chronic sleep restriction, CSR), and (2) whether
                      thepotential impact on GM plasticity depends on individual
                      differences in the availability of adenosinereceptors, which
                      are involved in mediating effects of caffeine on sleep and
                      waking function. Thirty‑six healthy adults participated in
                      this double‑blind, randomized, controlled study (age =
                      28.9 ± 5.2 y/;F:M = 15:21; habitual level of caffeine
                      intake < 450 mg; 29 homozygous C/C allele carriers of
                      rs5751876of ADORA2A, an A 2A adenosine receptor gene
                      variant). Each participant underwent a 9‑day
                      laboratoryvisit consisting of one adaptation day, 2 baseline
                      days (BL), 5‑day sleep restriction (5 h
                      time‑in‑bed),and a recovery day (REC) after an 8‑h
                      sleep opportunity. Nineteen participants received 300
                      mgcaffeine in coffee through the 5 days of CSR (CAFF group),
                      while 17 matched participants receiveddecaffeinated coffee
                      (DECAF group). We examined GM changes on the 2nd BL Day, 5th
                      CSR Day,and REC Day using magnetic resonance imaging and
                      voxel‑based morphometry. Moreover, we usedpositron
                      emission tomography with [ 18 F]‑CPFPX to quantify the
                      baseline availability of A 1 adenosinereceptors (A 1 R) and
                      its relation to the GM plasticity. The results from the
                      voxel‑wise multimodalwhole‑brain analysis on the
                      Jacobian‑modulated T1‑weighted images controlled for
                      variances of cerebral blood flow indicated a significant
                      interaction effect between caffeine and CSR in four
                      brainregions: (a) right temporal‑occipital region, (b)
                      right dorsomedial prefrontal cortex (DmPFC), (c)left
                      dorsolateral prefrontal cortex (DLPFC), and (d) right
                      thalamus. The post‑hoc analyses on the signalintensity of
                      these GM clusters indicated that, compared to BL, GM on the
                      CSR day was increasedin the DECAF group in all clusters but
                      decreased in the thalamus, DmPFC, and DLPFC in the
                      CAFFgroup. Furthermore, lower baseline subcortical A 1 R
                      availability predicted a larger GM reduction in theCAFF
                      group after CSR of all brain regions except for the
                      thalamus. In conclusion, our data suggest anadaptive GM
                      upregulation after 5‑day CSR, while concomitant use of
                      caffeine instead leads to a GMreduction. The lack of
                      consistent association with individual A 1 R availability
                      may suggest that CSR andcaffeine affect thalamic GM
                      plasticity predominantly by a different mechanism. Future
                      studies on therole of adenosine A 2A receptors in
                      CSR‑induced GM plasticity are warranted.},
      cin          = {INM-5 / INM-2},
      ddc          = {600},
      cid          = {I:(DE-Juel1)INM-5-20090406 / I:(DE-Juel1)INM-2-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {38830861},
      UT           = {WOS:001238391600069},
      doi          = {10.1038/s41598-024-61421-8},
      url          = {https://juser.fz-juelich.de/record/1030414},
}