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@ARTICLE{Tichelman:1014971,
      author       = {Tichelman, Naemi and Foerges, Anna L. and Elmenhorst,
                      Eva-Maria and Lange, Denise and Hennecke, Eva and Baur,
                      Diego M. and Beer, Simone and Kroll, Tina and Neumaier,
                      Bernd and Bauer, Andreas and Landolt, Hans-Peter and
                      Aeschbach, Daniel and Elmenhorst, David},
      title        = {{A} genetic variation in the adenosine {A}2{A} receptor
                      gene contributes to variability in oscillatory alpha power
                      in wake and sleep {EEG} and {A}1 adenosine receptor
                      availability in the human brain},
      journal      = {NeuroImage},
      volume       = {280},
      issn         = {1053-8119},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {FZJ-2023-03515},
      pages        = {120345 -},
      year         = {2023},
      abstract     = {The EEG alpha rhythm (∼ 8–13 Hz) is one of the most
                      salient human brain activity rhythms, modulated by the level
                      of attention and vigilance and related to cerebral energy
                      metabolism. Spectral power in the alpha range in wakefulness
                      and sleep strongly varies among individuals based on genetic
                      predisposition. Knowledge about the underlying genes is
                      scarce, yet small studies indicated that the variant
                      rs5751876 of the gene encoding A2A adenosine receptors
                      (ADORA2A) may contribute to the inter-individual variation.
                      The neuromodulator adenosine is directly linked to energy
                      metabolism as product of adenosine tri-phosphate breakdown
                      and acts as a sleep promoting molecule by activating A1 and
                      A2A adenosine receptors. We performed sleep and positron
                      emission tomography studies in 59 healthy carriers of
                      different rs5751876 alleles, and quantified EEG oscillatory
                      alpha power in wakefulness and sleep, as well as A1
                      adenosine receptor availability with 18F-CPFPX. Oscillatory
                      alpha power was higher in homozygous C-allele carriers (n =
                      27, 11 females) compared to heterozygous and homozygous
                      carriers of the T-allele (n(C/T) = 23, n(T/T) = 5, 13
                      females) (F(18,37) = 2.35, p = 0.014, Wilk's Λ = 0.487).
                      Furthermore, a modulatory effect of ADORA2A genotype on A1
                      adenosine receptor binding potential was found across all
                      considered brain regions (F(18,40) = 2.62, p = 0.006, Wilk's
                      Λ = 0.459), which remained significant for circumscribed
                      occipital region of calcarine fissures after correction for
                      multiple comparisons. In female participants, a correlation
                      between individual differences in oscillatory alpha power
                      and A1 receptor availability was observed. In conclusion, we
                      confirmed that a genetic variant of ADORA2A affects
                      individual alpha power, while a direct modulatory effect via
                      A1 adenosine receptors in females is suggested.},
      cin          = {INM-2 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37625500},
      UT           = {WOS:001070643100001},
      doi          = {10.1016/j.neuroimage.2023.120345},
      url          = {https://juser.fz-juelich.de/record/1014971},
}