Sleep deprivation, oxidative stress and inflammation

Atrooz, Fatin; Salim, Samina

doi:10.1016/bs.apcsb.2019.03.001

Cited by 121 publications

(103 citation statements)

References 139 publications

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“…Interestingly, the prefrontal cortex is especially susceptible to oxidative stress and furthermore, sleep deprivation especially affects neuropsychological performance on tasks related to the prefrontal cortex (executive domains) [ 36 ]. Thus, it is possible that grey matter health in dorsal-orbitofrontal areas is vulnerable to insufficient sleep [ 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

Specific cortical and subcortical grey matter regions are associated with insomnia severity

et al. 2021

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Background There is an increasing awareness that sleep disturbances are a risk factor for dementia. Prior case-control studies suggested that brain grey matter (GM) changes involving cortical (i.e, prefrontal areas) and subcortical structures (i.e, putamen, thalamus) could be associated with insomnia status. However, it remains unclear whether there is a gradient association between these regions and the severity of insomnia in older adults who could be at risk for dementia. Since depressive symptoms and sleep apnea can both feature insomnia-related factors, can impact brain health and are frequently present in older populations, it is important to include them when studying insomnia. Therefore, our goal was to investigate GM changes associated with insomnia severity in a cohort of healthy older adults, taking into account the potential effect of depression and sleep apnea as well. We hypothesized that insomnia severity is correlated with 1) cortical regions responsible for regulation of sleep and emotion, such as the orbitofrontal cortex and, 2) subcortical regions, such as the putamen. Methods 120 healthy subjects (age 74.8±5.7 years old, 55.7% female) were recruited from the Hillblom Healthy Aging Network at the Memory and Aging Center, UCSF. All participants were determined to be cognitively healthy following a neurological evaluation, neuropsychological assessment and informant interview. Participants had a 3T brain MRI and completed the Insomnia Severity Index (ISI), Geriatric Depression Scale (GDS) and Berlin Sleep Questionnaire (BA) to assess sleep apnea. Cortical thickness (CTh) and subcortical volumes were obtained by the CAT12 toolbox within SPM12. We studied the correlation of CTh and subcortical volumes with ISI using multiple regressions adjusted by age, sex, handedness and MRI scan type. Additional models adjusting by GDS and BA were also performed. Results ISI and GDS were predominantly mild (4.9±4.2 and 2.5±2.9, respectively) and BA was mostly low risk (80%). Higher ISI correlated with lower CTh of the right orbitofrontal, right superior and caudal middle frontal areas, right temporo-parietal junction and left anterior cingulate cortex (p<0.001, uncorrected FWE). When adjusting by GDS, right ventral orbitofrontal and temporo-parietal junction remained significant, and left insula became significant (p<0.001, uncorrected FWE). Conversely, BA showed no effect. The results were no longer significant following FWE multiple comparisons. Regarding subcortical areas, higher putamen volumes were associated with higher ISI (p<0.01). Conclusions Our findings highlight a relationship between insomnia severity and brain health, even with relatively mild insomnia, and independent of depression and likelihood of sleep apnea. The results extend the previous literature showing the association of specific GM areas (i.e, orbitofrontal, insular and temporo-parietal junction) not just with the presence of insomnia, but across the spectrum of severity itself. Moreover, our results suggest subcortical structures (i.e., putamen) are involved as well. Longitudinal studies are needed to clarify how these insomnia-related brain changes in healthy subjects align with an increased risk of dementia.

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Section: Discussionmentioning

confidence: 99%

Specific cortical and subcortical grey matter regions are associated with insomnia severity

et al. 2021

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“…In contrast, physical fatigue has many potential drivers (dehydration, glycogen depletion, muscle damage and mental fatigue), and recovery of muscle function is predominantly a matter of reversing the main causes of fatigue. Sleep deprivation (<7 h) increases circulating stress hormones (e.g., cortisol) [ 8 ]; decreases the regeneration of carbohydrate stores (i.e., glycogen) [ 9 ]; deregulates appetite and impacts on energy expenditure [ 10 ]; increases catabolism and reduces anabolism, impacting the rate of muscle repair (MPS) [ 11 , 12 ]. Therefore, sleep plays a key role in facilitation of post-exercise recovery or the reduction in fatigue and the reversal of the processes that lead to fatigue [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

The Sleep and Recovery Practices of Athletes

et al. 2021

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Background: Athletes maintain a balance between stress and recovery and adopt recovery modalities that manage fatigue and enhance recovery and performance. Optimal TST is subject to individual variance. However, 7–9 h sleep is recommended for adults, while elite athletes may require more quality sleep than non-athletes. Methods: A total of 338 (elite n = 115, 74 males and 41 females, aged 23.44 ± 4.91 years; and sub-elite n = 223, 129 males and 94 females aged 25.71 ± 6.27) athletes were recruited from a variety of team and individual sports to complete a battery of previously validated and reliable widely used questionnaires assessing sleep, recovery and nutritional practices. Results: Poor sleep was reported by both the elite and sub-elite athlete groups (i.e., global PSQI score ≥5—elite 64% [n = 74]; sub-elite 65% [n = 146]) and there was a significant difference in sport-specific recovery practices (3.22 ± 0.90 vs. 2.91 ± 0.90; p < 0.001). Relatively high levels of fatigue (2.52 ± 1.32), stress (1.7 ± 1.31) and pain (50%, n = 169) were reported in both groups. A range of supplements were used regularly by athletes in both groups; indeed, whey (elite n = 22 and sub-elite n = 48) was the most commonly used recovery supplement in both groups. Higher alcohol consumption was observed in the sub-elite athletes (12%, n = 26) and they tended to consume more units of alcohol per drinking bout. Conclusion: There is a need for athletes to receive individualised support and education regarding their sleep and recovery practices.

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“…These findings illustrated that hippocampal neuronal cells are susceptible to oxidative damage and that oxidative stress plays a pivotal role in cytotoxicity induced by sleep deprivation. Numerous reports have suggested that sleep deprivation triggers increased oxidative stress in the brain, causing damage to neuronal cells, which in turn leads to cognitive and memory dysfunction [ 60 , 61 ]. Na + /K + ATPase is highly sensitive to oxidative damage and free radical attack [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Successfully Rescues the Hippocampal Molecular Machinery and Enhances Anti-oxidative Activity Following Early-Life Sleep Deprivation Injury

et al. 2021

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Early-life sleep deprivation (ESD) is a serious condition with severe cognitive sequelae. Considering hippocampus plays an essential role in cognitive regulation, the present study aims to determine whether melatonin, a neuroendocrine beard with significant anti-oxidative activity, would greatly depress the hippocampal oxidative stress, improves the molecular machinery, and consequently exerts the neuro-protective effects following ESD. Male weanling Wistar rats (postnatal day 21) were subjected to ESD for three weeks. During this period, the animals were administered normal saline or melatonin (10 mg/kg) via intraperitoneal injection between 09:00 and 09:30 daily. After three cycles of ESD, the animals were kept under normal sleep/wake cycle until they reached adulthood and were sacrificed. The results indicated that ESD causes long-term effects, such as impairment of ionic distribution, interruption of the expressions of neurotransmitters and receptors, decreases in the levels of several antioxidant enzymes, and impairment of several signaling pathways, which contribute to neuronal death in hippocampal regions. Melatonin administration during ESD prevented these effects. Quantitative evaluation of cells also revealed a higher number of neurons in the melatonin-treated animals when compared with the saline-treated animals. As the hippocampus is critical to cognitive activity, preserving or even improving the hippocampal molecular machinery by melatonin during ESD not only helps us to better understand the underlying mechanisms of ESD-induced neuronal dysfunction, but also the therapeutic use of melatonin to counteract ESD-induced neuronal deficiency.

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Sleep deprivation, oxidative stress and inflammation

Cited by 121 publications

References 139 publications

Specific cortical and subcortical grey matter regions are associated with insomnia severity

Specific cortical and subcortical grey matter regions are associated with insomnia severity

The Sleep and Recovery Practices of Athletes

Melatonin Successfully Rescues the Hippocampal Molecular Machinery and Enhances Anti-oxidative Activity Following Early-Life Sleep Deprivation Injury

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