scholarly journals Physical Activity Modulates Common Neuroplasticity Substrates in Major Depressive and Bipolar Disorder

2017 ◽  
Vol 2017 ◽  
pp. 1-37 ◽  
Author(s):  
Cristy Phillips
Keyword(s):  
Physical Activity ◽  
Bipolar Disorder ◽  
Mood Disorders ◽  
Biogenic Amine ◽  
Clinical Utility ◽  
Major Depressive ◽  
Positive Effects ◽  
Mental Diseases

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.

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

2021 ◽  
Author(s):  
Lea Sirignano ◽  
Fabian Streit ◽  
Josef Frank ◽  
Lea Zillich ◽  
Stephanie Witt ◽  
...  
Keyword(s):  
Physical Activity ◽  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Circadian Rhythm ◽  
Mood Disorders ◽  
Genetic Correlations ◽  
Biological Rhythms ◽  
Moderate Activity ◽  
Healthy Controls ◽  
Major Depressive

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.

scholarly journals EEG Frontal Asymmetry in Dysthymia, Major Depressive Disorder and Euthymic Bipolar Disorder

Symmetry ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2414
Author(s):  
Chiara Spironelli ◽  
Francesca Fusina ◽  
Marco Bortolomasi ◽  
Alessandro Angrilli
Keyword(s):  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Quantitative Eeg ◽  
Beta Activity ◽  
Major Depressive ◽  
Eeg Asymmetry ◽  
Frontal Asymmetry ◽  
Frontal Eeg Asymmetry

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.

scholarly journals Age-Related Increase in the Number of Oligodendrocytes Is Dysregulated in Schizophrenia and Mood Disorders

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Victor Vostrikov ◽  
Natalya Uranova
Keyword(s):  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
White Matter ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Numerical Density ◽  
Major Depressive ◽  
Age Related ◽  
Related Increase

The postnatal maturation of the human prefrontal cortex is associated with substantial increase of number of oligodendrocytes. Previously, we reported decreased numerical density of oligodendrocytes in the prefrontal cortex in schizophrenia and mood disorders. To gain further understanding of the role oligodendrocytes in pathogenesis of schizophrenia and mood disorders, we examined the effect of the age on the number of oligodendrocytes in the prefrontal cortex in schizophrenia, bipolar disorder, and major depressive disorder. We revealed the age-related increase in numerical density of oligodendrocytes in layer VI and adjacent white matter of BA10 and BA 9 in normal controls but not in schizophrenia, bipolar disorder, and major depressive disorder. The absence of normal increase in the number of oligodendrocytes in gray and white matter with age in schizophrenia and mood disorders suggests that age-related process of oligodendrocyte increase is dysregulated in schizophrenia and mood disorders.

scholarly journals The genetics of the mood disorder spectrum: genome-wide association analyses of over 185,000 cases and 439,000 controls

2018 ◽  
Author(s):  
Jonathan R. I. Coleman ◽  
Héléna A. Gaspar ◽  
Julien Bryois ◽  
Gerome Breen ◽  
◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Major Depression ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Major Depressive ◽  
Genome Wide ◽  
Genome Wide Significance

AbstractBackgroundMood disorders (including major depressive disorder and bipolar disorder) affect 10-20% of the population. They range from brief, mild episodes to severe, incapacitating conditions that markedly impact lives. Despite their diagnostic distinction, multiple approaches have shown considerable sharing of risk factors across the mood disorders.MethodsTo clarify their shared molecular genetic basis, and to highlight disorder-specific associations, we meta-analysed data from the latest Psychiatric Genomics Consortium (PGC) genome-wide association studies of major depression (including data from 23andMe) and bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,285 cases, 439,741 controls; non-overlapping N = 609,424).ResultsSeventy-three loci reached genome-wide significance in the meta-analysis, including 15 that are novel for mood disorders. More genome-wide significant loci from the PGC analysis of major depression than bipolar disorder reached genome-wide significance. Genetic correlations revealed that type 2 bipolar disorder correlates strongly with recurrent and single episode major depressive disorder. Systems biology analyses highlight both similarities and differences between the mood disorders, particularly in the mouse brain cell types implicated by the expression patterns of associated genes. The mood disorders also differ in their genetic correlation with educational attainment – positive in bipolar disorder but negative in major depressive disorder.ConclusionsThe mood disorders share several genetic associations, and can be combined effectively to increase variant discovery. However, we demonstrate several differences between these disorders. Analysing subtypes of major depressive disorder and bipolar disorder provides evidence for a genetic mood disorders spectrum.

Mood (Affective) Disorders

2018 ◽  
pp. 15-60
Author(s):  
Carol S. North ◽  
Sean H. Yutzy
Keyword(s):  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Mood Disorders ◽  
Affective Disorders ◽  
Essential Feature ◽  
Severe Depression ◽  
Manic Episode ◽  
Major Depressive ◽  
Manic Symptoms ◽  
Mood Depression

Descriptions of mood disorders go back to the time of Hippocrates. Mood disorders are primarily characterized by depressed and/or elevated (manic) moods. The essential feature of mood disorders is an episode that is a distinct and persistent change from a person’s typical mood (depression or mania), accompanied by other depressive and manic symptoms, lasting 2 weeks for a major depressive episode and 1 week for a manic episode. Such episodes typically remit and recur over the course of time. Manic episodes define bipolar disorder. Severe depression without manic episodes is diagnosed as major depressive disorder. Mood disorders present a 10- to 30-fold risk for suicide. Effective treatments for mood disorders include medications, brain stimulation modalities, and psychotherapy.

Mood Disorders

2017 ◽  
Author(s):  
Harvinder Singh ◽  
Brian Frankel
Keyword(s):  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Major Depressive ◽  
Bipolar Ii Disorder ◽  
Bipolar I Disorder ◽  
Bipolar Ii ◽  
Cyclothymic Disorder ◽  
Persistent Depressive Disorder

In this chapter the topics that are reviewed include major depressive disorder, persistent depressive disorder (dysthymia), unspecified depressive disorder, bipolar I disorder, bipolar II disorder, cyclothymic disorder and unspecified bipolar disorder

scholarly journals Second messenger/signal transduction pathways in major mood disorders: moving from membrane to mechanism of action, part II: bipolar disorder

CNS Spectrums ◽  
2013 ◽  
Vol 18 (5) ◽  
pp. 242-251 ◽  
Author(s):  
Mark J. Niciu ◽  
Dawn F. Ionescu ◽  
Daniel C. Mathews ◽  
Erica M. Richards ◽  
Carlos A. Zarate
Keyword(s):  
Signal Transduction ◽  
Bipolar Disorder ◽  
Mood Disorders ◽  
Second Messenger ◽  
Pharmacological Interventions ◽  
Major Depressive ◽  
The Past ◽  
Kinase C ◽  
Gsk 3Β ◽  
Intracellular Mediators

In this second of two articles on second messenger/signal transduction cascades in major mood disorders, we will review the evidence in support of intracellular dysfunction and its rectification in the etiopathogenesis and treatment of bipolar disorder (BD). The importance of these cascades is highlighted by lithium's (the gold standard in BD psychopharmacology) ability to inhibit multiple critical loci in second messenger/signal transduction cascades including protein kinase C (involved in the IP3/PIP2 pathway) and GSK-3β (canonically identified in the Wnt/Fz/Dvl/GSK-3β cascade). As a result, and like major depressive disorder (MDD), more recent pathophysiological studies and rational therapeutic targets have been directed at these and other intracellular mediators. Even in the past decade, intracellular dysfunction in numerous neuroprotective/apoptotic cascades appears important in the pathophysiology and may be a future target for pharmacological interventions of BD.

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