Sleep and slow-wave activity in depressed adolescent boys: a preliminary study

Santangeli, Olena; Porkka‐Heiskanen, Tarja; Virkkala, Jussi; Castaneda, Anu E.; Marttunen, Mauri; Paunio, T.; Urrila, Anna S.

doi:10.1016/j.sleep.2017.06.029

Cited by 18 publications

(14 citation statements)

References 73 publications

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“…It is postulated that the decrease in SWA during the course of sleep is associated with reduced synaptic strength and is thus related to memory consolidation [51]. Our previous results on the same sample of adolescents indicated that this SWA dissipation that occurs normally during healthy sleep is affected by depression and related sleep disturbances [23]. The results of the current study further propose a link between SWA dissipation and changes in methylation of the Protein Phosphatase 2 regulatory subunit B'gamma (PPP2RC5).…”

Section: Discussionsupporting

confidence: 64%

“…Different sleep disturbances can therefore affect LTP and LTD differently [56,66]. Since in our sample there was no marked difference in REM sleep between cases and controls [23], it is plausible that there were no differences in LTP genetic pathways either.…”

Section: Discussionmentioning

confidence: 69%

“…Polysomnography was performed for two consecutive nights and, for the purposes of this study, the first night (adaptation night) was discarded and the second night of polysomnography was used in the analyses. One of the most important functional parameters of the sleeping EEG, slow wave sleep (SWA), was calculated using a power spectral analysis according to a previously described procedure [23]. Because in previous work with the same sample of adolescents we detected a flattening of SWA dissipation associated with depression especially in the frontal electrodes [23], we also wanted to explore its effect on methylation in this study.…”

Section: Assessment Of Sleepmentioning

confidence: 99%

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Epigenetic dysregulation of genes related to synaptic long-term depression among adolescents with depressive disorder and sleep symptoms

et al. 2019

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Objectives: This study aimed to test the hypothesis that sleep and depression have independent effects on brain development and plasticity in adolescents, and that these changes are reflected in changes in the epigenome. Methods: Participants were 17 medication-free adolescent boys (age 16.05 ± 0.80 years, mean ± standard deviation (SD); eight cases with depression and sleep symptoms, nine healthy controls). Sleep was assessed by polysomnography recordings and the Pediatric Daytime Sleepiness Scale (PDSS) and Athens Insomnia Scale (AIS). Participants underwent a clinical evaluation. DNA methylation of blood leukocytes was measured by Illumina 450K array, and Ingenuity Pathway analysis was applied to identify the most significant pathways with differentially methylated positions (DMPs). Secondary analysis of the identified loci included linear correlations between methylation and the subjectively rated scales of sleep, depression and sleep microarchitecture. Results: Due to small sample size, we found no genome-wide significant differences in methylation between cases and controls. However, pathway analysis identified the synaptic long-term depression (LTD) canonical pathway (p ¼ 0.00045) when the best 500 DMPs from the original caseecontrol design were included. A flattened dissipation of slow wave sleep, tiredness and depression severity values correlated with five of 10 sites from the LTD pathway (IGF1R, PLAG16, PLA2R1, PPP2C5 and ERK12) in the secondary analysis when the caseecontrol status was controlled for. Conclusion: Among adolescents, depressive disorder with sleep symptoms is associated with a distinctive epigenetic pattern of DNA methylation in blood leukocytes. The enrichment of DMPs on genes related to synaptic LTD emphasizes the role of sleep in synaptic plasticity and the widespread physiological consequences of disturbed sleep.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 69%

Section: Assessment Of Sleepmentioning

confidence: 99%

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Epigenetic dysregulation of genes related to synaptic long-term depression among adolescents with depressive disorder and sleep symptoms

et al. 2019

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“…EEG signals can be analyzed by linear and non-linear dynamic analyses. Linear analysis such as power spectrum is commonly used to extract the features of sleep EEG signals [13,26,40,44]. Spectral characteristic parameters can reflect the energy information transported by each frequency band.…”

Section: Introductionmentioning

confidence: 99%

Spatio-temporal dynamics of EEG features during sleep in major depressive disorder after treatment with escitalopram: a pilot study

Wang

Yang

et al. 2020

BMC Psychiatry

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Background: Previous studies have shown escitalopram is related to sleep quality. However, effects of escitalopram on dynamics of electroencephalogram (EEG) features especially during different sleep stages have not been reported. This study may help to reveal pharmacological mechanism underlying escitalopram treatment. Methods: The spatial and temporal responses of patients with major depressive disorder (MDD) to escitalopram treatment were analyzed in this study. Eleven MDD patients and eleven healthy control subjects who completed eight weeks' treatment of escitalopram were included in the final statistics. Six-channel sleep EEG signals were acquired during sleep. Power spectrum and nonlinear dynamics were used to analyze the spatio-temporal dynamics features of the sleep EEG after escitalopram treatment. Results: For temporal dynamics: after treatment, there was a significant increase in the relative energy (RE) of δ 1 band (0.5-2 Hz), accompanied by a significant decrease in the RE of β 2 band (20-30 Hz). Lempel-Ziv complexity and Co-complexity values were significantly lower. EEG changes at different sleep stages also showed the same regulation as throughout the night sleep. For spatio dynamics: after treatment, the EEG response of the left and right hemisphere showed asymmetry. Regarding band-specific EEG complexity estimations, δ1 and β2 in stage-1 and δ1 in stage-2 sleep stage in frontal cortex is found to be much more sensitive to escitalopram treatment in comparison to central and occipital cortices. Conclusions: The sleep quality of MDD patients improved, EEG response occurred asymmetry in left and right hemispheres due to escitalopram treatment, and frontal cortex is found to be much more sensitive to escitalopram treatment. These findings may contribute to a comprehensive understanding of the pharmacological mechanism of escitalopram in the treatment of depression.

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“…This discrepancy might be explained mainly by the considerably longer follow-up time in our current study, as well as the differing methods for assessing sleep abnormalities (objective sleep EEG vs. subjective reports). Polysomnographic studies in MDD point overall towards alterations in sleep continuity, sleep depth, and REM sleep pressure [30,31], the findings being less consistent and less severe among children and adolescents than among adults [30][31][32]. In turn, subjective sleep complaints among depressed adolescents include insomnia or hypersomnia, experiences of insufficient sleep quality, and daytime sleepiness [29,31].…”

Section: Discussionmentioning

confidence: 99%

Sleep symptoms and long-term outcome in adolescents with major depressive disorder: a naturalistic follow-up study

Urrila

Kiviruusu

Haravuori

et al. 2019

Eur Child Adolesc Psychiatry

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Sleep abnormalities in major depressive disorder (MDD) have been suggested to represent a vulnerability trait, which might predispose the individual to long-term psychiatric morbidity. In this study, we sought to assess whether the presence of sleep symptoms among adolescents with MDD is associated with poorer long-term outcome in young adulthood during naturalistic follow-up. Adolescent outpatients diagnosed with MDD (n = 166; age 13-19 years, 17.5% boys) were followed up during 8 years in naturalistic settings. N = 112 adolescents (16.1% boys) completed the 8-year assessment. Sleep symptoms and psychosocial functioning were assessed with structured clinical interviews, and depressive and anxiety symptoms with questionnaires. The severity of sleep symptoms at baseline was not associated with worse outcome at 8 years in terms of any of the outcome measures tested. In particular, the presence of a disturbed sleep-wake rhythm at baseline was associated with a more favourable outcome at 8 years: less depression and anxiety symptoms and higher level of psychosocial functioning. The presence of sleep symptoms in young adulthood was associated with the presence of current depression and anxiety symptoms and poorer psychosocial functioning. The presence of sleep symptoms at follow-up seems to be state-dependent: they are observed in conjunction with other psychiatric symptoms. Contrary to our hypothesis, our results suggest that sleep complaints among adolescents with MDD do not lead to poorer long-term clinical outcome in young adulthood. The link between sleep-wake rhythm disturbance and better long-term outcome needs to be confirmed and examined in detail in further studies, but here we speculate about possible explanations.

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Sleep and slow-wave activity in depressed adolescent boys: a preliminary study

Cited by 18 publications

References 73 publications

Epigenetic dysregulation of genes related to synaptic long-term depression among adolescents with depressive disorder and sleep symptoms

Epigenetic dysregulation of genes related to synaptic long-term depression among adolescents with depressive disorder and sleep symptoms

Spatio-temporal dynamics of EEG features during sleep in major depressive disorder after treatment with escitalopram: a pilot study

Sleep symptoms and long-term outcome in adolescents with major depressive disorder: a naturalistic follow-up study

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