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

CNS Spectrums ◽  
2013 ◽  
Vol 18 (5) ◽  
pp. 231-241 ◽  
Author(s):  
Mark J. Niciu ◽  
Dawn F. Ionescu ◽  
Daniel C. Mathews ◽  
Erica M. Richards ◽  
Carlos A. Zarate
Keyword(s):  
Signal Transduction ◽  
Major Depressive Disorder ◽  
Amino Acid ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Mechanism Of Action ◽  
Time Lag ◽  
Second Messenger ◽  
Mood Stabilizers ◽  
Major Depressive

The etiopathogenesis and treatment of major mood disorders have historically focused on modulation of monoaminergic (serotonin, norepinephrine, dopamine) and amino acid [γ-aminobutyric acid (GABA), glutamate] receptors at the plasma membrane. Although the activation and inhibition of these receptors acutely alter local neurotransmitter levels, their neuropsychiatric effects are not immediately observed. This time lag implicates intracellular neuroplasticity as primary in the mechanism of action of antidepressants and mood stabilizers. The modulation of intracellular second messenger/signal transduction cascades affects neurotrophic pathways that are both necessary and sufficient for monoaminergic and amino acid–based treatments. In this review, we will discuss the evidence in support of intracellular mediators in the pathophysiology and treatment of preclinical models of despair and major depressive disorder (MDD). More specifically, we will focus on the following pathways: cAMP/PKA/CREB, neurotrophin-mediated (MAPK and others), p11, Wnt/Fz/Dvl/GSK3β, and NFκB/ΔFosB. We will also discuss recent discoveries with rapidly acting antidepressants, which activate the mammalian target of rapamycin (mTOR) and release of inhibition on local translation via elongation factor stimulation. Throughout this discourse, we will highlight potential intracellular targets for therapeutic intervention. Finally, future clinical implications are discussed.

Augmentation strategies in the treatment of major depressive disorder

2016 ◽  
Vol 33 (S1) ◽  
pp. S407-S407
Author(s):  
S. Bise ◽  
B. Kurtovic ◽  
D. Begic ◽  
O. Cemalovic
Keyword(s):  
Major Depressive Disorder ◽  
Combination Therapy ◽  
Depressive Disorder ◽  
Mood Stabilizers ◽  
Augmentation Therapy ◽  
Major Depressive ◽  
Augmentation Strategies ◽  
Significant Difference ◽  
Augmentation Strategy ◽  
Competing Interest

Augmentation strategies for the treatment of Major depressive disorder (MDD) are needed when patients with MDD have a partial, or not responded to antidepressant monotherapy. The focus of augmentation therapy has been combining an antidepressant (AD) medication with another AD. Atypical antipsychotics (AAP) are becoming commonly used to augment antidepressants. Beyond AD and AAP, alternative augmentation strategies include mood stabilizers (MS).AimTo analyze the characteristics of therapy in patients with diagnosis of MDD and to investigate the frequency of augmentation therapy.MethodStudy included 28 patients hospitalized during one year with MDD diagnosis. Statistical analysis was performed with x2 and t-test.ResultAmong patients with MDD there were 18 (64.28%) women with an average age 57.5 and 10 (35.71%) men with an average age 53.5. Of the 28 patients with MDD, 25 (89.28%) were treated with a combination therapy, and monotherapy in the remaining 3 patients (10.71%). Of 25 patients with augmentation strategy treatment, 22 (88%) used two medications and the remaining 3 (12%) tree psychotropic medications (AAP, AD, MS). The most frequent combinations were a combination of AD and AAP (17 patients, 68%). Beyond that frequent combination were AD and MS (6 patients, 24%). Two patients used combination two AAP, and one patient with two AD and one patients used AAP and MS.ConclusionAugmentation strategy is often used in patients with MDD. There is no significant difference in the use combination therapy based on gender and age.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Cortical Thickness in Individuals at High Familial Risk of Mood Disorders as They Develop Major Depressive Disorder

2015 ◽  
Vol 78 (1) ◽  
pp. 58-66 ◽  
Author(s):  
Martina Papmeyer ◽  
Stephen Giles ◽  
Jessica E. Sussmann ◽  
Shauna Kielty ◽  
Tiffany Stewart ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Cortical Thickness ◽  
Familial Risk ◽  
Major Depressive

Family study of the aggregation of eating disorders and mood disorders

2003 ◽  
Vol 33 (7) ◽  
pp. 1319-1323 ◽  
Author(s):  
B. MANGWETH ◽  
J. I. HUDSON ◽  
H. G. POPE ◽  
A. HAUSMANN ◽  
C. De COL ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Family Study ◽  
Familial Aggregation ◽  
Interview Study ◽  
Major Depressive ◽  
Causal Factors ◽  
Family Interview

Background. Family studies have suggested that eating disorders and mood disorders may coaggregate in families. To study further this question, data from a family interview study of probands with and without major depressive disorder was examined.Method. A bivariate proband predictive logistic regression model was applied to data from a family interview study, conducted in Innsbruck, Austria, of probands with (N=64) and without (N=58) major depressive disorder, together with 330 of their first-degree relatives.Results. The estimated odds ratio (OR) for the familial aggregation of eating disorders (anorexia nervosa, bulimia nervosa and binge-eating disorder) was 7·0 (95% CI 1·4, 28; P=0·006); the OR for the familial aggregation of mood disorders (major depression and bipolar disorder) was 2·2 (0·92, 5·4; P=0·076); and for the familial coaggregation of eating disorders with mood disorders the OR was 2·2 (1·1, 4·6; P=0·035).Conclusions. The familial coaggregation of eating disorders with mood disorders was significant and of the same magnitude as the aggregation of mood disorders alone – suggesting that eating disorders and mood disorders have common familial causal factors.

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.

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