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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 Subsequently, caffeine was withdrawn and repeated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},
}