scholarly journals Restoration of psychosocial functioning in remitted major depressive disorder patients: A 1-year longitudinal study

2020 ◽  
Vol 102 ◽  
pp. 152204
Author(s):  
Zhenzhen Wang ◽  
Haitao Qu ◽  
Jiaqi Zhong ◽  
Yang Han ◽  
Cheng Wan ◽  
...  
2021 ◽  
Vol 89 (9) ◽  
pp. S161
Author(s):  
Andrew Cutler ◽  
Scott T. Aaronson ◽  
Gregory W. Mattingly ◽  
Samuel T. Wilkinson ◽  
Robert Lasser ◽  
...  

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.


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