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(searched for: <p>Effects of Sleep Deprivation on Brain Functional Network</p>)
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Vivianne Jakobsson
Published: 17 February 2020
Abstract: Introduction:
Sleep
deprivation
is a common problem that may have serious consequences. In this study,
functional
magnetic resonance imaging (fMRI), a technique frequently used to study
networks
in the
brain
, was used to investigate the resting state
of
the
sleep
deprived
brain
, in order to discover whether this state affects the intrinsic connectivity and the global signal variability (GSV). Aims: To investigate whether GSV increases with
sleep
deprivation
. Material and Methods: In this cross over study 18 healthy participants, age 20 – 30, underwent in randomized order resting-state fMRI for 20min before and after 24h
sleep
deprivation
. We extracted the global signal, calculated the standard deviation per participant, and analysed it with respect to
sleep
depraved yes/no, head motion, eyes open/closed and self-evaluation
of
sleepiness using Karolinska Sleepiness Score (KSS). Results: We found that GSV was higher during
sleep
deprivation
(0.3362 ± 0.0241,
p<0.0001)
without KSS data. With KSS,
sleep
deprivation
was not significant (0.0619 ± 0.1145,
p
=0.5889). High KSS rating had a significant
effect
on
GSV (0.1497 ± 0.0409,
p
=0.0003), as had head motion (1.7974 ± 0.1539,
p<0.0001).
There was no significant difference between having eyes open or closed (0.0126 ± 0.0578,
p
=0.8278), and no significant increase for each time period
of
20s in the scanner (0.0065 ± 0.0021,
p
=0.0029). Conclusions: We found that the global signal variation is increased by
sleep
deprivation
and sleepiness. More specific conclusions cannot be made from our data so far.
Jonathan Nowak, Annika Dimitrov, Nicole Y.L. Oei, Henrik Walter, Mazda Adli, Sciprofile linkIlya M. Veer
Published: 24 January 2020
Psychoneuroendocrinology, Volume 114; doi:10.1016/j.psyneuen.2020.104585

The publisher has not yet granted permission to display this abstract.
Sciprofile linkSandro Franceschini, Matteo Lulli, Sara Bertoni, Simone Gori, Alessandro Angrilli, Martina Mancarella, Giovanna Puccio, Andrea Facoetti
Published: 3 October 2019
Journal of Psychopharmacology, Volume 34, pp 315-325; doi:10.1177/0269881119878178

The publisher has not yet granted permission to display this abstract.
Sciprofile linkM. W. DiFrancesco, T. Van Dyk, M. Altaye, S.
P
. A. Drummond, D. W. Beebe
Scientific Reports, Volume 9, pp 13913-13; doi:10.1038/s41598-019-50180-6

Abstract: Neuroimaging studies
of
the Psychomotor Vigilance Task (PVT) have revealed
brain
regions involved in attention lapses in
sleep-deprived
and well-rested adults. Those studies have focused
on
individual
brain
regions, rather than integrated
brain
networks
, and have overlooked adolescence, a period
of
ongoing
brain
development and endemic short
sleep
. This study used
functional
MRI (fMRI) and a contemporary analytic approach to assess time-resolved peri-stimulus response
of
key
brain
networks
when adolescents complete the PVT, and test for differences across attentive versus inattentive periods and after short
sleep
versus well-rested states. Healthy 14-17-year-olds underwent a within-subjects randomized protocol including 5-night spans
of
extended versus short
sleep
. PVT was performed during fMRI the morning after each
sleep
condition. Event-related independent component analysis (eICA) identified coactivating
functional
networks
and corresponding time courses. Analysis
of
salient time course characteristics tested the
effects
of
sleep
condition, lapses, and their interaction. Seven eICA
networks
were identified supporting attention, executive control, motor, visual, and default-mode
functions
. Attention lapses, after either
sleep
manipulation, were accompanied by broadly increased response magnitudes post-stimulus and delayed peak responses in some
networks
. Well-circumscribed
networks
respond during the PVT in adolescents, with timing and intensity impacted by attentional lapses regardless
of
experimentally shortened or extended
sleep
.
Liwei Zhang, Yue Huang, Ying Zhang, Wei Xin, Sciprofile linkYongcong Shao, Sciprofile linkYebing Yang
Published: 1 August 2019
NeuroImage, Volume 197, pp 255-263; doi:10.1016/j.neuroimage.2019.04.057

The publisher has not yet granted permission to display this abstract.
Frank Raven, Sciprofile linkPeter Meerlo, Y A. Van Der Zee, Sciprofile linkTed Abel, Sciprofile linkRobbert Havekes
Neurobiology of Learning and Memory, Volume 160, pp 83-90; doi:10.1016/j.nlm.2018.03.018

Abstract:
Sleep
and
sleep
loss have a profound impact
on
hippocampal
function
, leading to memory impairments. Modifications in the strength
of
synaptic connections directly influences neuronal communication, which is vital for normal
brain
function
, as well as the processing and storage
of
information. In a recently published study, we found that as little as five hours
of
sleep
deprivation
impaired hippocampus-dependent memory consolidation, which was accompanied by a reduction in dendritic spine numbers in hippocampal area CA1. Surprisingly, loss
of
sleep
did not alter the spine density
of
CA3 neurons. Although
sleep
deprivation
has been reported to affect the
function
of
the dentate gyrus, it is unclear whether a brief period
of
sleep
deprivation
impacts spine density in this region. Here, we investigated the impact
of
a brief period
of
sleep
deprivation
on
dendritic structure in the dentate gyrus
of
the dorsal hippocampus. We found that five hours
of
sleep
loss reduces spine density in the dentate gyrus with a prominent
effect
on
branched spines. Interestingly, the inferior blade
of
the dentate gyrus seems to be more vulnerable in terms
of
spine loss than the superior blade. This decrease in spine density predominantly in the inferior blade
of
the dentate gyrus may contribute to the memory deficits observed after
sleep
loss, as structural reorganization
of
synaptic
networks
in this subregion is fundamental for cognitive processes.
Rui Zhao, Xinxin Zhang, Yuanqiang Zhu, Ningbo Fei, Jinbo Sun, Peng Liu, Xuejuan Yang, Sciprofile linkWei Qin
Published: 1 February 2019
Neuroscience, Volume 398, pp 37-54; doi:10.1016/j.neuroscience.2018.11.049

The publisher has not yet granted permission to display this abstract.
Wenhao Chen, Jie Chen, Xiao Lin, Peng Li, Le Shi, Jia-Jia Liu, Hong-Qiang Sun, Sciprofile linkLin Lu, Sciprofile linkJie Shi
Published: 1 October 2018
Sleep Medicine, Volume 50, pp 137-144; doi:10.1016/j.sleep.2018.05.040

The publisher has not yet granted permission to display this abstract.
Bo Ma, Jincheng Chen, Yongying Mu, Bingjie Xue, Aimei Zhao, Daoping Wang, Dennis Chang, Sciprofile linkYinghong Pan, Jianxun Liu
Published: 20 September 2018
PLOS ONE, Volume 13; doi:10.1371/journal.pone.0199237

Abstract:
Sleep
is an essential and fundamental physiological process that plays crucial roles in the balance
of
psychological and physical health.
Sleep
disorder may lead to adverse health outcomes. The
effects
of
sleep
deprivation
were extensively studied, but its mechanism is still not fully understood. The present study aimed to identify the alterations
of
serum proteins associated with chronic
sleep
deprivation
, and to seek for potential biomarkers
of
sleep
disorder mediated diseases. A label-free quantitative proteomics technology was used to survey the global changes
of
serum proteins between normal rats and chronic
sleep
deprivation
rats. A total
of
309 proteins were detected in the serum samples and among them, 117 proteins showed more than 1.8-folds abundance alterations between the two groups.
Functional
enrichment and
network
analyses
of
the differential proteins revealed a close relationship between chronic
sleep
deprivation
and several biological processes including energy metabolism, cardiovascular
function
and nervous
function
. And four proteins including pyruvate kinase M1, clusterin, kininogen1 and profilin-1were identified as potential biomarkers for chronic
sleep
deprivation
. The four candidates were validated via parallel reaction monitoring (PRM) based targeted proteomics. In addition, protein expression alteration
of
the four proteins was confirmed in myocardium and
brain
of
rat model. In summary, the comprehensive proteomic study revealed the biological impacts
of
chronic
sleep
deprivation
and discovered several potential biomarkers. This study provides further insight into the pathological and molecular mechanisms underlying
sleep
disorders at protein level.
Shanaz Diessler, Maxime Jan, Yann Emmenegger, Nicolas Guex, Benita Middleton, Sciprofile linkDebra J. Skene, Mark Ibberson, Frederic Burdet, Lou Götz, Sciprofile linkMarco Pagni, et al.
Published: 9 August 2018
PLOS Biology, Volume 16; doi:10.1371/journal.pbio.2005750

Abstract:
Sleep
is essential for optimal
brain
functioning
and health, but the biological substrates through which
sleep
delivers these beneficial
effects
remain largely unknown. We used a systems genetics approach in the BXD genetic reference population (GRP)
of
mice and assembled a comprehensive experimental knowledge base comprising a deep "
sleep
-wake" phenome, central and peripheral transcriptomes, and plasma metabolome data, collected under undisturbed baseline conditions and after
sleep
deprivation
(SD). We present analytical tools to interactively interrogate the database, visualize the molecular
networks
altered by
sleep
loss, and prioritize candidate genes. We found that a one-time, short disruption
of
sleep
already extensively reshaped the systems genetics landscape by altering 60%-78%
of
the transcriptomes and the metabolome, with numerous genetic loci affecting the magnitude and direction
of
change. Systems genetics integrative analyses drawing
on
all levels
of
organization imply α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking and fatty acid turnover as substrates
of
the negative
effects
of
insufficient
sleep
. Our analyses demonstrate that genetic heterogeneity and the
effects
of
insufficient
sleep
itself
on
the transcriptome and metabolome are far more widespread than previously reported.
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