IL-1β and BDNF are associated with improvement in hypersomnia but not insomnia following exercise in major depressive disorder.

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hypersomnia 82 Title: Translational PsychiatryIL-1β and BDNF are associated with improvement in hypersomnia but not insomnia following exercise in major depressive disorderAlternative Title: Biomarkers and sleep
hypersomnia 708 crucial to improve treatment outcomes. Sleep disturbances are varied and can present as insomnia and/or hypersomnia . Though research has examined the biological underpinnings of insomnia in MDD, little is known about
hypersomnia 847 examined the biological underpinnings of insomnia in MDD, little is known about the role of biomarkers in hypersomnia associated with MDD. This paper examines biomarkers associated with changes in hypersomnia and insomnia
hypersomnia 938 biomarkers in hypersomnia associated with MDD. This paper examines biomarkers associated with changes in hypersomnia and insomnia and as predictors of improvements in sleep quality following exercise augmentation in persons
hypersomnia 1422 Depressive Symptomatology (sleep onset insomnia, mid-nocturnal insomnia, early morning insomnia and hypersomnia ) assessed self-reported sleep quality. Inflammatory cytokines (tumor necrosis factor-alpha, interleukin
hypersomnia 1700 were assessed in blood samples collected before and following the 12-week intervention. Reduction in hypersomnia was correlated with reductions in BDNF (ρ=0.26, P=0.029) and IL-1β (ρ=0.37, P=0.002). Changes in
hypersomnia 2017 were predictive of greater improvements in insomnia (F=3.87, P=0.050). In conclusion, improvement in hypersomnia is related to reductions in inflammatory markers and BDNF in persons with non-remitted MDD. Distinct
hypersomnia 3569 in IL-1β and TNF-α can impair sleep.[11], [12]Sleep disturbances can present as either insomnia or hypersomnia in MDD, with hypersomnia as a defining symptom of atypical depression. Distinguishing between atypical
hypersomnia 3594 impair sleep.[11], [12]Sleep disturbances can present as either insomnia or hypersomnia in MDD, with hypersomnia as a defining symptom of atypical depression. Distinguishing between atypical and melancholic depression
hypersomnia 3995 biological correlates of sleep disturbances is limited in that it does not distinguish between insomnia and hypersomnia . Identification of biomarkers that uniquely predict or correlate with improvements in hypersomnia and
hypersomnia 4093 and hypersomnia. Identification of biomarkers that uniquely predict or correlate with improvements in hypersomnia and insomnia is an important step toward more effective treatment of MDD.Exercise has proven efficacious
hypersomnia 4632 of this paper is to identify biological correlates and predictors of improvements in self-reported hypersomnia and insomnia through a secondary analysis of the Treatment with Exercise Augmentation for Depression
hypersomnia 4923 decreases in pro-inflammatory cytokines will be associated with improvements in self-reported insomnia and hypersomnia and (2) baseline levels of these biomarkers will predict improvements in self-reported insomnia and
hypersomnia 5035 and (2) baseline levels of these biomarkers will predict improvements in self-reported insomnia and hypersomnia .Materials and methodsThe TREAD trial was a randomized trial comparing two doses of aerobic exercise
hypersomnia 7256 sleep-related items on the IDS-C (sleep onset insomnia, mid-nocturnal insomnia, early morning insomnia and hypersomnia ) were used to assess self-reported sleep quality. Each sleep item was scored on a scale of 0–3, with
hypersomnia 9387 correlation coefficient was used to examine the relationship between change in each biomarker and change in hypersomnia and insomnia. Change variables (week 12—baseline) were only calculated for subjects who provided week
hypersomnia 9668 model repeated-measures analysis examined the relationship between each baseline cytokine level and hypersomnia and insomnia over the 12-week study period. Each model contained fixed effects terms for baseline biomarker
hypersomnia 10430 analysis of the TREAD data (Trivedi 2011). Covariates included in the model were baseline insomnia or hypersomnia , IDS-C score minus sleep items, family history of MDD, recurrent MDD, age, sex, race, body mass index,
hypersomnia 11714 2 presents the mean change in depressive symptoms (IDS-C total score), IDS-C total insomnia, IDS-C hypersomnia and each biomarker. Spearman correlation coefficients between the change in each biomarker and changes
hypersomnia 11845 Spearman correlation coefficients between the change in each biomarker and changes in insomnia and hypersomnia are presented in Table 3. In summary, there was a significant correlation between change in IL-1β and
hypersomnia 11970 in Table 3. In summary, there was a significant correlation between change in IL-1β and change in hypersomnia (ρ=−0.37, P=0.003) and between change in BDNF and change in hypersomnia (ρ=0.26, P=0.029). No other
hypersomnia 12045 in IL-1β and change in hypersomnia (ρ=−0.37, P=0.003) and between change in BDNF and change in hypersomnia (ρ=0.26, P=0.029). No other correlations were significant.Baseline biomarkers as predictors of change
hypersomnia 12822 indicate a relationship between changes in inflammatory and neurotrophic biomarkers and changes in hypersomnia in a study of exercise augmentation for non-remitted MDD. Specifically, reductions in BDNF and IL-1β
hypersomnia 12965 augmentation for non-remitted MDD. Specifically, reductions in BDNF and IL-1β are related to reductions in hypersomnia . Furthermore, low baseline levels of IL-1β were predictive of greater reductions in insomnia during
hypersomnia 13875 to examine this relationship in subjects with MDD. The relationship of reduced IL-1β with reduced hypersomnia fits with previous research. Though IL-1β is generally thought to enhance sleep, extreme increases
hypersomnia 14985 improvements in sleep quality following exercise, as decreases in BDNF were associated with decreased hypersomnia . This finding is in contrast to our initial hypothesis that improvements in sleep would be related to
hypersomnia 15760 between our results and our initial hypothesis may be owing to the unique biological underpinnings of hypersomnia and help further highlight the possible differential biomarker associations between hypersomnia and
hypersomnia 15856 of hypersomnia and help further highlight the possible differential biomarker associations between hypersomnia and insomnia.Hypersomnia is a symptom most commonly associated with atypical depression. Atypical depression
hypersomnia 16790 BDNF production. In this scenario, decreased BDNF production would be associated with decreases in hypersomnia , which matches our findings.There was no relationship between changes in these inflammatory markers
hypersomnia 17762 tolerance.[52], [53]The associations of inflammatory and neurotrophic markers with an improvement in hypersomnia but not insomnia provide further support for the differing biological underpinnings of atypical depression.
hypersomnia 19435 mechanisms are likely involved. The fact that changes in IL-1β and BDNF were only related to changes in hypersomnia further support the need to identify biological markers that differentiate across different symptom
hypersomnia 20125 (years)10547.51 (9.44) Female (%)10580 IDS-C10534.14 (7.25) IDS insomnia1054.25 (2.18)4.00 (3.00–6.00)IDS hypersomnia 1050.67 (0.90)0.00 (0.00–1.00)BDNF10419.06 (6.23)18.04 (14.96–22.91)IL-1β1030.10 (0.07)0.08 (0.06–0.13)IL-61050.80
hypersomnia 21409 coefficients (rs) between the change in each inflammatory cytokine level and change in insomnia and hypersomnia BDNFIL-6TNF-αIL-1β nρP-valuenρP-valuenρP-valuenρP-valueInsomnia68−0.090.481700.050.64270−0.040.73167−0.030.802Hypersomnia680.260.029700.050.674700.080.511670.370.002Abbreviations:

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