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| 100 | 1 | _ | |a Lin, Yu-Shiuan |0 P:(DE-Juel1)180805 |b 0 |e Corresponding author |
| 245 | _ | _ | |a Repeated caffeine intake suppresses cerebral grey matter responses to chronic sleep restriction in an A1 adenosine receptor-dependent manner: a double-blind randomized controlled study with PET-MRI |
| 260 | _ | _ | |a [London] |c 2024 |b Macmillan Publishers Limited, part of Springer Nature |
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| 500 | _ | _ | |a 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 |
| 520 | _ | _ | |a 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. |
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