Psychosocial Functioning in Youths at High Risk to Develop Major Depressive Disorder

Author(s):  
BORIS BIRMAHER ◽  
JEFFREY A. BRIDGE ◽  
DOUGLAS E. WILLIAMSON ◽  
DAVID A. BRENT ◽  
RONALD E. DAHL ◽  
...  
2021 ◽  
pp. 102883
Author(s):  
Neslihan ALTUNSOY ◽  
Didem SÜCÜLLÜOĞLU DİKİCİ ◽  
Fikret Poyraz ÇÖKMÜŞ ◽  
Hüseyin Murat ÖZKAN ◽  
Kadir AŞÇIBAŞI ◽  
...  

BJPsych Open ◽  
2021 ◽  
Vol 7 (S1) ◽  
pp. S300-S300
Author(s):  
Michael Weightman ◽  
Bernhard Baune

AimsThis poster aims to examine the impact of social cognitive deficits on psychosocial functioning in depressed patients, as well as summarise the utility of various evidence-based therapeutic interventions employed to target these deficits. The stated hypotheses were twofold: (1) that social cognitive impairment in major depressive disorder will correlate with poorer psychosocial functioning; and (2) that these deficits will respond to existing anti-depressant therapies.BackgroundSocial cognition is an important adaptive trait that incorporates the identification, perception and interpretation of socially relevant information from the external world. It is frequently affected in major depressive disorder such that depressed patienMethodA review of the existing literature was performed in order to test the stated hypotheses. Pertinent sources were identified via the MEDLINE, EMBASE, PsycINFO, PubMed, Scopus and Google Scholar databases. A total of 107 studies met inclusion criteria for review.ResultImpaired social cognitive performance in depressed patients correlated with poorer psychosocial functioning across the key domains of general cognitive functioning and quality of life. Many current anti-depressant therapies were found to have a normalising effect on the social cognitive abilities of depressed subjects, both at a neural and functional level. Anti-depressant medications, in particular citalopram and reboxetine, appeared to correct facial affect recognition deficits, while a psychotherapeutic approach demonstrated improvements in theory of mind and negative interpretive bias. Data relating to other common treatments, such as electroconvulsive therapy, are limited.ConclusionThe impact and treatment of social cognitive deficits in major depressive disorder is an important emerging field. The social cognitive deficits evident in depressed patients are sometimes subtle, but afford a significant functional impact. Additionally, it appears these impairments are at least partially reversible using anti-depressants or psychotherapy.


2020 ◽  
Vol 34 (12) ◽  
pp. 1443-1448
Author(s):  
Cleo Desormeaux ◽  
Fanny Demars ◽  
Elisabeth Davenas ◽  
Therese M Jay ◽  
Francis Lavergne

Background: Major depressive disorder is a common illness that severely decreases psychosocial functioning. Due to the major limitations of current treatments including response failure, it is crucial to develop better therapy strategies. Evidence suggests that dopamine dysregulation might play a major role in major depressive disorder physiopathology. Aims: This study investigates whether the dopamine D1 receptor agonist A77636 modulates antidepressant-like activity in rats. Methods: Rats were injected with an acute single dose of A77636 (0.75, 1.5 or 3 mg/kg), a potent and selective dopamine D1-like receptor agonist. Their locomotor activity, social interactions and behavioural response to the forced swim test were analysed 30 min after the injection. Results: During the forced swim test, the D1 agonist dose dependently reduced the immobility while the time of bursting was increased. Social interactions were significantly increased in the animals exposed to 3 mg/kg of A77636 whereas no significant changes were measured in general motor activity. Conclusions: The present results provide evidence that pharmacological modulation of D1 receptor by the selective agonist A77636 induces antidepressant-like effects in rats, which encourages further studies regarding D1-specific modulation in major depressive disorder treatment.


2000 ◽  
Vol 57 (9) ◽  
pp. 867 ◽  
Author(s):  
Boris Birmaher ◽  
Ronald E. Dahl ◽  
Douglas E. Williamson ◽  
James M. Perel ◽  
David A. Brent ◽  
...  

2016 ◽  
Vol 46 (11) ◽  
pp. 2351-2361 ◽  
Author(s):  
T. Nickson ◽  
S. W. Y. Chan ◽  
M. Papmeyer ◽  
L. Romaniuk ◽  
A. Macdonald ◽  
...  

BackgroundPrevious neuroimaging studies indicate abnormalities in cortico-limbic circuitry in mood disorder. Here we employ prospective longitudinal voxel-based morphometry to examine the trajectory of these abnormalities during early stages of illness development.MethodUnaffected individuals (16–25 years) at high and low familial risk of mood disorder underwent structural brain imaging on two occasions 2 years apart. Further clinical assessment was conducted 2 years after the second scan (time 3). Clinical outcome data at time 3 was used to categorize individuals: (i) healthy controls (‘low risk’, n = 48); (ii) high-risk individuals who remained well (HR well, n = 53); and (iii) high-risk individuals who developed a major depressive disorder (HR MDD, n = 30). Groups were compared using longitudinal voxel-based morphometry. We also examined whether progress to illness was associated with changes in other potential risk markers (personality traits, symptoms scores and baseline measures of childhood trauma), and whether any changes in brain structure could be indexed using these measures.ResultsSignificant decreases in right amygdala grey matter were found in HR MDD v. controls (p = 0.001) and v. HR well (p = 0.005). This structural change was not related to measures of childhood trauma, symptom severity or measures of sub-diagnostic anxiety, neuroticism or extraversion, although cross-sectionally these measures significantly differentiated the groups at baseline.ConclusionsThese longitudinal findings implicate structural amygdala changes in the neurobiology of mood disorder. They also provide a potential biomarker for risk stratification capturing additional information beyond clinically ascertained measures.


2020 ◽  
Author(s):  
Richard Neugebauer ◽  
Priya Wickramaratne ◽  
Connie Svob ◽  
Clayton McClintock ◽  
Marc J. Gameroff ◽  
...  

Background. In most studies, religiosity and spirituality (R/S) are positively associated with altruism, whereas depression is negatively associated. However, the cross-sectional designs of these studies limit their epidemiological value. We examine the association of R/S and major depressive disorder (MDD) with altruism in a five year longitudinal study nested in a larger prospective study.Methods. Depressed and non-depressed individuals and their first- and second-generation offspring were assessed over several decades. At Year30 after baseline, R/S was measured using participants’ self-report; MDD, by clinical interview. At Year35, participants completed a measure of altruism. Adjusted odds ratios (AOR) were calculated using multivariate logistic regression; statistical significance, set at p<.05. two-tailed.Results. In the overall sample, both R/S and MDD were significantly associated with altruism, AOR 2.52 (95% CI 1.15-5.49) and AOR 2.43 (95% CI 1.05-5.64), respectively; in the High Risk group alone, the corresponding AORs were 4.69 (95% CI 1.39-15.84) and 4.74 (95% CI 1.92-11.72). Among highly R/S people in the High Risk group, the AOR for MDD with altruism was 22.55 (95% CI 1.23-414.60) p<.04; among the remainder, it was 3.12 (95% CI 0.63-15.30), a substantial but non-significant difference.Limitations. Altruism is based on self-report, not observation, hence, vulnerable to bias.Conclusions. MDD’s positive association with elevated altruism concurs with studies of posttraumatic growth in finding developmental growth from adversity. The conditions that foster MDD’s positive association with altruism and the contribution of R/S to this process requires further study.


2014 ◽  
Vol 75 (12) ◽  
pp. 1359-1370 ◽  
Author(s):  
Vanessa C. Evans ◽  
Grant L. Iverson ◽  
Lakshmi N. Yatham ◽  
Raymond W. Lam

2012 ◽  
Vol 43 (4) ◽  
pp. 673-687 ◽  
Author(s):  
S. Cohen-Woods ◽  
I. W. Craig ◽  
P. McGuffin

BackgroundIt has been well established that both genes and non-shared environment contribute substantially to the underlying aetiology of major depressive disorder (MDD). A comprehensive overview of genetic research in MDD is presented.MethodPapers were retrieved from PubMed up to December 2011, using many keywords including: depression, major depressive disorder, genetics, rare variants, gene–environment, whole genome, epigenetics, and specific candidate genes and variants. These were combined in a variety of permutations.ResultsLinkage studies have yielded some promising chromosomal regions in MDD. However, there is a continued lack of consistency in association studies, in both candidate gene and genome-wide association studies (GWAS). Numerous factors may account for variable results including the use of different diagnostic approaches, small samples in early studies, population stratification, epigenetic phenomena, copy number variation (CNV), rare variation, and phenotypic and allelic heterogeneity. The conflicting results are also probably, in part, a consequence of environmental factors not being considered or controlled for.ConclusionsEach research group has to identify what issues their sample may best address. We suggest that, where possible, more emphasis should be placed on the environment in molecular behavioural genetics to identify individuals at environmental high risk in addition to genetic high risk. Sequencing should be used to identify rare and alternative variation that may act as a risk factor, and a systems biology approach including gene–gene interactions and pathway analyses would be advantageous. GWAS may require even larger samples with reliably defined (sub)phenotypes.


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