Major Depressive Disorder and Bipolar Disorder Subtypes Differ in their Genetic Correlations with Physical Activity, Circadian Rhythm, and Sleep

Author(s):  
Lea Sirignano ◽  
Fabian Streit ◽  
Josef Frank ◽  
Lea Zillich ◽  
Stephanie Witt ◽  
...  

Abstract Alterations in biological rhythms are features of mood disorders. Patients suffering from major depressive disorder (MDD) show decreased physical activity compared to healthy controls. Bipolar disorder (BIP) patients differ in their activity patterns during different mood phases, and in comparison to their non-affected relatives and healthy controls. In both MDD and BIP, circadian rhythms can be disrupted, accompanied by sleep problems and changes in sleep duration. It is unclear whether the observed associations are due to common etiology or if they are influenced by the current mood state in which they are observed. Here, we used summary statistics from large-scale genome-wide association analysis (GWAS) to test the genetic correlations of MDD, BIP-I, and BIP-II with physical activity (overall physical activity, moderate activity, sedentary behavior), circadian rhythm (relative amplitude) and sleep features (sleep duration, daytime sleepiness). MDD showed positive genetic correlations with sedentary behavior, and negative correlations with overall physical activity and moderate activity, while BIP-I showed associations in the opposite direction. MDD and BIP-II had negative genetic correlations with relative amplitude. All mood disorders were positively genetically correlated with daytime sleepiness. The correlational patterns show that MDD and BIP-I differ the most in their correlations with biological rhythms with BIP-II seemingly occupying a intermediate position. Furthermore, our results suggest that the clinically observed associations between mood disorders and biological rhythms have shared genetic underpinnings. Future research considering possible joint mechanisms may offer potential avenues for improving disease detection and treatment.

2012 ◽  
Vol 4 ◽  
pp. CMPsy.S7989 ◽  
Author(s):  
Daniel P. Cardinali ◽  
María F. Vidal ◽  
Daniel E. Vigo

Circadian rhythm abnormalities, as shown by sleep/wake cycle disturbances, constitute one the most prevalent signs of depressive illness; advances or delays in the circadian phase are documented in patients with major depressive disorder (MDD), bipolar disorder, and seasonal affective disorder (SAD). The disturbances in the amplitude and phase of rhythm in melatonin secretion that occur in patients with depression resemble those seen in chronobiological disorders, thus suggesting a link between disturbed melatonin secretion and depressed mood. Based on this, agomelatine, the first MT1/MT2 melatonergic agonist displaying also 5-HT2C serotonergic antagonism, has been introduced as an antidepressant. Agomelatine has been shown to be effective in several animal models of depression and anxiety and it has beneficial effects in patients with MDD, bipolar disorder, or SAD. Among agomelatine's characteristics are a rapid onset of action and a pronounced effectiveness for correcting circadian rhythm abnormalities and improving the sleep/wake cycle. Agomelatine also improves the 3 functional dimensions of depression—emotional, cognitive, and social—thus aiding in the full recovery of patients to a normal life.


2017 ◽  
Vol 2017 ◽  
pp. 1-37 ◽  
Author(s):  
Cristy Phillips

Mood disorders (MDs) are chronic, recurrent mental diseases that affect millions of individuals worldwide. Although the biogenic amine model has provided some clinical utility, a need remains to better understand the interrelated mechanisms that contribute to neuroplasticity deficits in MDs and the means by which various therapeutics mitigate them. Of those therapeutics being investigated, physical activity (PA) has shown clear and consistent promise. Accordingly, the aims of this review are to (1) explicate key modulators, processes, and interactions that impinge upon multiple susceptibility points to effectuate neuroplasticity deficits in MDs; (2) explore the putative mechanisms by which PA mitigates these features; (3) review protocols used to induce the positive effects of PA in MDs; and (4) highlight implications for clinicians and researchers.


Symmetry ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2414
Author(s):  
Chiara Spironelli ◽  
Francesca Fusina ◽  
Marco Bortolomasi ◽  
Alessandro Angrilli

In the last few decades, the incidence of mood disorders skyrocketed worldwide and has brought an increasing human and economic burden. Depending on the main symptoms and their evolution across time, they can be classified in several clinical subgroups. A few psychobiological indices have been extensively investigated as promising markers of mood disorders. Among these, frontal asymmetry measured at rest with quantitative EEG has represented the main available marker in recent years. Only a few studies so far attempted to distinguish the features and differences among diagnostic types of mood disorders by using this index. The present study measured frontal EEG asymmetry during a 5-min resting state in three samples of patients with bipolar disorder in a Euthymic phase (EBD, n = 17), major depressive disorder (MDD, n = 25) and persistent depressive disorder (PDD, n = 21), once termed dysthymia. We aimed to test the hypothesis that MDD and PDD lack the typical leftward asymmetry exhibited by normal as well as EBD patients, and that PDD shows greater clinical and neurophysiological impairments than MDD. Clinical scales revealed no symptoms in EBD, and significant larger anxiety and depression scores in PDD than in MDD patients. Relative beta (i.e., beta/alpha ratio) EEG asymmetry was measured from lateral frontal sites and results revealed the typical greater left than right frontal beta activity in EBD, as well as a lack of asymmetry in both MDD and PDD. The last two groups also had lower bilateral frontal beta activity in comparison with the EBD group. Results concerning group differences were interpreted by taking into account both the clinical and the neurophysiological domains.


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