Dataset Information

?-Amyloid accumulation in the human brain after one night of sleep deprivation.

ABSTRACT: The effects of acute sleep deprivation on ?-amyloid (A?) clearance in the human brain have not been documented. Here we used PET and 18F-florbetaben to measure brain A? burden (ABB) in 20 healthy controls tested after a night of rested sleep (baseline) and after a night of sleep deprivation. We show that one night of sleep deprivation, relative to baseline, resulted in a significant increase in A? burden in the right hippocampus and thalamus. These increases were associated with mood worsening following sleep deprivation, but were not related to the genetic risk (APOE genotype) for Alzheimer's disease. Additionally, baseline ABB in a range of subcortical regions and the precuneus was inversely associated with reported night sleep hours. APOE genotyping was also linked to subcortical ABB, suggesting that different Alzheimer's disease risk factors might independently affect ABB in nearby brain regions. In summary, our findings show adverse effects of one-night sleep deprivation on brain ABB and expand on prior findings of higher A? accumulation with chronic less sleep.

SUBMITTER: Shokri-Kojori E

PROVIDER: S-EPMC5924922 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

β-Amyloid accumulation in the human brain after one night of sleep deprivation.

Shokri-Kojori Ehsan E Wang Gene-Jack GJ Wiers Corinde E CE Demiral Sukru B SB Guo Min M Kim Sung Won SW Lindgren Elsa E Ramirez Veronica V Zehra Amna A Freeman Clara C Miller Gregg G Manza Peter P Srivastava Tansha T De Santi Susan S Tomasi Dardo D Benveniste Helene H Volkow Nora D ND

Proceedings of the National Academy of Sciences of the United States of America 20180409 17

The effects of acute sleep deprivation on β-amyloid (Aβ) clearance in the human brain have not been documented. Here we used PET and <sup>18</sup>F-florbetaben to measure brain Aβ burden (ABB) in 20 healthy controls tested after a night of rested sleep (baseline) and after a night of sleep deprivation. We show that one night of sleep deprivation, relative to baseline, resulted in a significant increase in Aβ burden in the right hippocampus and thalamus. These increases were associated with mood ...[more]

PMID: 29632177

Similar Datasets

Project description:Sleep insufficiency is associated with various disorders (cardiovascular disease, neurodegenerative diseases, immunological disorders.) but the molecular bases for these associations are largely unknown. We used multiple omics techniques to examine changes in the blood of healthy male and female adults voluntarily subjected to 24 h of sleep deprivation followed by up to one day of recovery with normal sleep routines. Thirty-two (14 males, 18 females) healthy adults 22-27 years old donated fasting blood samples prior to (Day 1) and following (Days 2 and 3) a 24-hour period of sleep deprivation. Blood samples were subjected to cell, biochemical, transcriptomic, proteomic and metabolomic analyses. Multi-omics integration analysis showed that sleep deprivation caused marked molecular changes (46.4% transcript genes, 59.3% proteins and 55.6% metabolites) that had not been restored by Day 2. Transient sleep deprivation had the greatest impact on the immune system and, in particular, on neutrophil-mediated immune processes. Correlation analysis with neutrophils suggested the plasma level of superoxidase dismustase-1 (SOD1) and the primary blood mononuclear cell transcriptional profile of the S100A8 gene could be used as biomarkers reflecting the sleep deprivation-associated disordered immunological state. An increased number of immune cells (leukocytes, neutrophils, monocytes, eosinophils, CD4+T), inflammatory factors (TNF-α, INF-γ, Il-6, IL-10, IL-12) and c-reactive protein in blood plasma further demonstrated the dysregulation of the immune system associated with short-term sleep deprivation. Other important findings associated with sleep deprivation included a significant decrease in the plasma melatonin level and an enrichment of molecules in signaling pathways associated with brain disorders, including schizophrenia and neurodegenerative diseases. Taken in concert, these points suggest that disrupted sleep, such as may occur in shift work, perturbs immunological status and may increase the risk for brain disorders in later life.

Project description:Background: Sleep loss contributes to obesity through a variety of mechanisms, including neuroendocrine functioning, increased hunger, and increased food intake. Additionally, sleep loss alters functional activation within brain regions associated with reward and behavioral control. However, it remains unknown whether individual differences in baseline neural functioning can predict eating behaviors during total sleep deprivation (TSD). We used functional magnetic resonance imaging (fMRI) to test the hypothesis that individuals with increased baseline responsiveness within reward regions are more vulnerable to TSD-induced overeating. Methods: N = 45 subjects completed several fMRI scans during a single pre-TSD session that included performance on the Multi-Source Interference Task (MSIT) and the n-back task. Subjects returned to the laboratory for an overnight TSD session, during which they were given ad libitum access to 10,900 kcal of food. Leftover food and packaging were collected every 6 h (00:00, 06:00, and 12:00) to measure total food consumption. Subjects reported sleepiness every hour and performed a food rating task every 3 h. Results: Functional activation within the ventral striatum during the MSIT and n-back positively correlated with total caloric and carbohydrate intake during the final 6 h (06:00-12:00) of TSD. Activation within the middle and superior temporal gyri during the MSIT also correlated with total carbohydrates consumed. Food consumption did not correlate with subjective sleepiness, hunger, or food desire. Conclusions: Individual differences in neural activity of reward processing areas (i.e., nucleus accumbens) prior to sleep deprivation are associated with an individual's propensity to overeat during subsequent sleep deprivation. This suggests that individual differences within reward processing pathways are potential key factors in sleep loss related overeating. Sleep loss and obesity are tightly linked. Both phenomena have been associated with increased neural activation in regions associated with reward, inhibitory control, and disrupted dopamine signaling. Elevated baseline reward sensitivity in the ventral striatum appears to be further compounded by sleep deprivation induced dysfunction in the reward neurocircuitry, increasing the likelihood of overeating. Our findings suggest that large individual differences in baseline responsiveness of hedonic reward pathways may modulate the association between sleep loss and obesity.

Dataset Information

?-Amyloid accumulation in the human brain after one night of sleep deprivation.

Publications

β-Amyloid accumulation in the human brain after one night of sleep deprivation.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets