Seasonal variation in mood among individuals with and without bipolar disorder.

Introduction: Bipolar disorder is a disorder characterized by cyclic changes in mood, yet limited research has explored longitudinal patterns of seasonality on mood symptoms in this population. This study aimed to examine longitudinal mood symptoms in individuals with bipolar type I and II, and healthy controls to determine if seasonal patterns were present and to validate the Global Seasonality Score as a measure of seasonality.

Methods: Participants from the Prechter Longitudinal Study of Bipolar Disorder were included.

Antidepressant effects of acute sleep deprivation are reduced in highly controlled environments.

Background: Numerous studies summarized in a recent meta-analysis have shown sleep deprivation rapidly improves depressive symptoms in approximately 50 % of individuals with major depressive disorder (MDD), however those studies were typically conducted in clinical settings. Here we investigated the effects of sleep deprivation utilizing a highly controlled experimental approach.

Methods: 36 antidepressant-free individuals with MDD and 10 healthy controls (HC) completed a 5 day/4-night protocol consisting of adaptation, baseline, total sleep deprivation (TSD), and recovery phases.

Enhanced amygdala-cingulate connectivity associates with better mood in both healthy and depressive individuals after sleep deprivation.

Sleep loss robustly disrupts mood and emotion regulation in healthy individuals but can have a transient antidepressant effect in a subset of patients with depression. The neural mechanisms underlying this paradoxical effect remain unclear. Previous studies suggest that the amygdala and dorsal nexus (DN) play key roles in depressive mood regulation.

Does insomnia treatment prevent depression?

Rates of major depressive disorder (MDD) are increasing globally, in part due to the coronavirus disease 2019 pandemic, contributing to disease burden. It has long been known that insomnia is intricately connected with depression as indicated by greater depression severity and lower treatment response. Furthermore, insomnia is a significant risk factor for new-onset depression.

The sleep homeostatic response to sleep deprivation in humans is heritable.

Study Objectives: Following sleep deprivation, increases in delta power have historically been used to index increases in sleep pressure. Research in mice has demonstrated that the homeostatic delta power response to sleep deprivation is heritable. Whether this is true in humans is unknown.

Treatment of Insomnia with Zaleplon in HIV+ Significantly Improves Sleep and Depression.

More than 50% of individuals who are HIV positive report insomnia, which can reduce HIV treatment adherence, impair quality of life, and contribute to metabolic dysfunction. Major depressive disorder is also highly comorbid in this population, leading to further impairment. There is evidence that treating insomnia may improve not only sleep, but depression and metabolic function, as well.

A preliminary study on the relationship between sleep, depression and cardiovascular dysfunction in a 4 sample population.

Background: Major Depressive Disorder (MDD) has been linked in the literature to poorer prognosis in patients with cardiovascular dysfunction, although the mechanisms of this relationship remain unclear. Underlying Sleep Disordered Breathing (SDB) serves as a potential candidate to explain this effect due to its downstream effects on inflammatory activation and decreased nitric oxide (NO) bioavailability, both of which have been shown to contribute to the pathophysiology of both MDD and cardiovascular disease (CVD).

Methods: This study utilizes overnight polysomnography and an inflammation panel to examine the links between cardiovascular dysfunction and sleep difficulties in control participants and patients diagnosed with SDB only, MDD only, and both SDB and MDD.

Spindles are highly heritable as identified by different spindle detectors.

Study Objectives: Sleep spindles, a defining feature of stage N2 sleep, are maximal at central electrodes and are found in the frequency range of the electroencephalogram (EEG) (sigma 11-16 Hz) that is known to be heritable. However, relatively little is known about the heritability of spindles. Two recent studies investigating the heritability of spindles reported moderate heritability, but with conflicting results depending on scalp location and spindle type.

An Integrated Sleep and Reward Processing Model of Major Depressive Disorder.

Major depressive disorder with comorbid sleep disturbance has been associated with negative outcomes, including lower rates of treatment response and a greater likelihood of depressive relapse compared to those without sleep disturbance. However, little, if any, research has been conducted to understand why such negative treatment outcomes occur when sleep disturbance is present. In this conceptual review, we argue that the relationship of sleep disturbance and negative treatment outcomes may be mediated by alterations in neural reward processing in individuals with blunted trait-level reward responsivity.

Precision Medicine for Insomnia.

Insomnia affects up to 15% of the US population. There are effective pharmacologic and behavioral treatments for insomnia; however, there is often no one-size-fits-all intervention. This article discusses the leading behavioral treatment of insomnia, cognitive behavioral therapy for insomnia, and its ability to be tailored to an individual's specific symptoms.

A preliminary investigation of the role of slow-wave activity in modulating waking EEG theta as a marker of sleep propensity in major depressive disorder.

Background: Both EEG slow-wave activity (SWA) during sleep and EEG theta activity during waking have been shown to increase with extended waking, and decrease following sleep, suggesting that both are markers of sleep propensity. In individuals with major depressive disorder (MDD), however, altered patterns of SWA have been noted, suggesting that sleep homeostasis is dysregulated. This study aimed to examine if slow-wave disruption would alter sleep propensity differently in healthy controls (HC) and those with MDD.

An Integrated Model of Slow-Wave Activity and Neuroplasticity Impairments in Major Depressive Disorder.

Purpose Of Review: In this review, we aim to integrate the most recent research highlighting alterations in sleep slow-wave activity (SWA), and impairments in neuroplasticity in major depressive disorder (MDD) into a novel model of disorder maintenance.

Recent Findings: Sleep homeostasis has been shown to be impaired in MDD, with a subset of individuals also demonstrating impaired SWA. SWA is considered a marker of the homeostatic regulation of sleep, and is implicated in the downscaling of synaptic strength in the context of maintaining homeostatic plasticity.

Effects of slow-wave activity on mood disturbance in major depressive disorder.

Background: Studies have demonstrated that decreases in slow-wave activity (SWA) predict decreases in depressive symptoms in those with major depressive disorder (MDD), suggesting that there may be a link between SWA and mood. The aim of the present study was to determine if the consequent change in SWA regulation following a mild homeostatic sleep challenge would predict mood disturbance.

Methods: Thirty-seven depressed and fifty-nine healthy adults spent three consecutive nights in the sleep laboratory.

Slow-wave disruption enhances the accessibility of positive memory traces.

The purpose of this study was to explore the effects of slow-wave disruption on positive and negative word recognition in a sample of healthy control participants and those with major depressive disorder. Prior to sleep, participants learned a set of emotional and neutral words during an encoding task by responding whether or not the word described them. Following baseline sleep, participants underwent one night of selective slow-wave disruption by auditory stimuli.

The role of fast and slow EEG activity during sleep in males and females with major depressive disorder.

Sleep difficulties are highly prevalent in depression, and appear to be a contributing factor in the development and maintenance of symptoms. However, despite the generally acknowledged relationship between sleep and depression, the neurophysiological substrates underlying this relationship still remain unclear. Two main hypotheses were tested in this study.

Reduction in delta activity predicted improved negative affect in Major Depressive Disorder.

While prior research has demonstrated a paradoxical antidepressant effect of slow-wave disruption (SWD), the specific dimensions of depression affected is still unclear. The current study aimed to extend this research by utilizing a dimensional approach in examining the antidepressant effects of SWD. Of particular interest is the affective dimension, as negative affect in depression is arguably the most salient characteristic of depression.

Examining the effects of sleep delay on depressed males and females and healthy controls.

Individuals with major depressive disorder typically exhibit sleep electroencephalograpy abnormalities which have been shown to vary by sex. Recent research has shown that depressed males display deficits in slow wave sleep and delta electroencephalograph (EEG) activity that are not apparent in depressed females. This may suggest that males and females with depression vary with respect to their homeostatic regulation of sleep.