Cognitive dysfunction in major depressive disorder: effects on psychosocial functioning and implications for treatment.
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ABSTRACT:
SUBMITTER: Lam RW
PROVIDER: S-EPMC4304584 | biostudies-literature | 2014 Dec
REPOSITORIES: biostudies-literature
Publications
Cognitive dysfunction in major depressive disorder: effects on psychosocial functioning and implications for treatment.
Lam Raymond W RW Kennedy Sidney H SH Mclntyre Roger S RS Khullar Atul A
Canadian journal of psychiatry. Revue canadienne de psychiatrie 20141201 12
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Project description:BackgroundCognitive impairment associated with lifetime major depressive disorder (MDD) is well-supported by meta-analytic studies, but population-based estimates remain scarce. Previous UK Biobank studies have only shown limited evidence of cognitive differences related to probable MDD. Using updated cognitive and clinical assessments in UK Biobank, this study investigated population-level differences in cognitive functioning associated with lifetime MDD.MethodsAssociations between lifetime MDD and cognition (performance on six tasks and general cognitive functioning [g-factor]) were investigated in UK Biobank (N-range 7,457-14,836, age 45-81 years, 52% female), adjusting for demographics, education, and lifestyle. Lifetime MDD classifications were based on the Composite International Diagnostic Interview. Within the lifetime MDD group, we additionally investigated relationships between cognition and (a) recurrence, (b) current symptoms, (c) severity of psychosocial impairment (while symptomatic), and (d) concurrent psychotropic medication use.ResultsLifetime MDD was robustly associated with a lower g-factor (β = -0.10, PFDR = 4.7 × 10-5), with impairments in attention, processing speed, and executive functioning (β ≥ 0.06). Clinical characteristics revealed differential profiles of cognitive impairment among case individuals; those who reported severe psychosocial impairment and use of psychotropic medication performed worse on cognitive tests. Severe psychosocial impairment and reasoning showed the strongest association (β = -0.18, PFDR = 7.5 × 10-5).ConclusionsFindings describe small but robust associations between lifetime MDD and lower cognitive performance within a population-based sample. Overall effects were of modest effect size, suggesting limited clinical relevance. However, deficits within specific cognitive domains were more pronounced in relation to clinical characteristics, particularly severe psychosocial impairment.
| S-EPMC7315876 | biostudies-literature
Project description:Background: Cognitive and psychosocial dysfunction are prevalent and disabling features of Major Depressive Disorder (MDD). Emerging evidence suggests that poor cognitive functioning mediates the negative effect of MDD on psychosocial function. However, there is a lack of research examining the domain-specific nature of this relationship. The current study evaluated whether the relationship between MDD and specific psychosocial subdomains (e.g., autonomy, occupational functioning) was mediated by domain-specific cognitive deficits. Methods: Data from 155 participants was obtained from the Cognitive Function and Mood Study (CoFaMS), a cross-sectional analysis of mood, cognition, social cognition, and functioning in individuals with MDD. Cognitive functioning was assessed (Current MDD n = 45, Healthy n = 110), with the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), the Colorado Assessment Tests (CATs), and the Psychology Experiment Building Language (PEBL). Psychosocial functioning was clinically evaluated with the Functioning Assessment Short Test (FAST). Results: The results indicated that spatial cognition and executive functioning partially mediated the negative effect of MDD on overall psychosocial functioning, autonomy, and subjective cognition. In contrast, spatial and executive domains showed divergent mediation patterns on interpersonal relationships and leisure time. Conclusions: The findings suggest that executive and spatial cognition play an important role in the pathology of overall psychosocial functioning, and specific functional issues in MDD. Treatments targeting psychosocial recovery in MDD may be improved by emphasizing executive and spatial cognitive remediation.
| S-EPMC6215806 | biostudies-literature
Project description:ObjectivesCompared with the general population, patients with major depressive disorder (MDD) report substantial deficits in their functioning that often go beyond the clinical resolution of depressive symptoms. This study examines the impact of MDD and its treatment on functioning.MethodsFrom the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, we analyzed complete data of 2280 adult outpatients with MDD at entry and exit points of each level of antidepressant treatment and again 12 months post treatment. Functioning was measured using the Work and Social Adjustment Scale (WSAS).ResultsThe results show that only 7% of patients with MDD reported within-normal functioning before treatment. The proportion of patients achieving within-normal functioning (WSAS) scores significantly increased after treatment. However, the majority of patients (>60%) were still in the abnormal range on functioning at exit. Although remitted patients had greater improvements compared with nonremitters, a moderate proportion of remitted patients continued to experience ongoing deficits in functioning after treatment (20-40%). Follow-up data show that the proportions of patients experiencing normal scores for functioning after 12 months significantly decreased from the end of treatment to the follow-up phase, from 60.1% to 49% (p < 0.0001), a finding that was particularly significant in nonremitters. Limitations of this study include the reliance on self-report of functioning and the lack of information on patients who dropped out.ConclusionThis study points to the importance of functional outcomes of MDD treatment as well as the need to develop personalized interventions to improve functioning in MDD.
| S-EPMC4907070 | biostudies-literature
Project description:Background: Recent evidence suggests that depressed patients experience social cognitive deficits (e.g., poor affect recognition). However, very little is known regarding the contribution of social cognitive deficits to psychosocial dysfunction (e.g., occupational functioning). In particular, the mechanistic roles of depression severity and cognitive deficits (e.g., memory) in this domain have not been explored. The current study evaluated the extent to which mood symptoms and cognitive deficits provide a mechanistic explanation for the relationship between social cognitive and psychosocial deficits in major depressive disorder (MDD). Methods: Data were obtained from 111 participants with MDD (75 Female, mean age = 35, 84% Caucasian, 12% Asian, 4% Other) in the Cognitive Function and Mood Study (CoFaM-S), a cross-sectional study of mood, social cognition, cognition, and psychosocial functioning in mood disorders. Social cognitive abilities were assessed using the Social Perception subtest of the Wechsler Adult Intelligence Scale, and psychosocial dysfunction was clinically evaluated with the Functioning Assessment Short Test (FAST). Results: Cognitive deficits and mood symptoms did not significantly mediate relationships between social cognitive ability and psychosocial dysfunction. The exception was executive function, which mediated an indirect relationship between meaning interpretation (i.e., theory of mind) and self-perceived cognitive dysfunction. Conclusion: The results suggest that the relationship between social cognitive deficits and psychosocial dysfunction is not mechanistically explained by mood symptoms or nonsocial cognition. Development of treatment strategies targeting social cognitive deficits in patients with MDD is warranted.
| S-EPMC6533355 | biostudies-literature
Project description:BackgroundMajor depressive disorder afflicts an estimated 17% of individuals during their lifetimes at tremendous suffering and costs. Cognitive therapy may be an effective treatment option for major depressive disorder, but the effects have only had limited assessment in systematic reviews.Methods/principal findingsCochrane systematic review methodology, with meta-analyses and trial sequential analyses of randomized trials, are comparing the effects of cognitive therapy versus 'treatment as usual' for major depressive disorder. To be included the participants had to be older than 17 years with a primary diagnosis of major depressive disorder. Altogether, we included eight trials randomizing a total of 719 participants. All eight trials had high risk of bias. Four trials reported data on the 17-item Hamilton Rating Scale for Depression and four trials reported data on the Beck Depression Inventory. Meta-analysis on the data from the Hamilton Rating Scale for Depression showed that cognitive therapy compared with 'treatment as usual' significantly reduced depressive symptoms (mean difference -2.15 (95% confidence interval -3.70 to -0.60; P<0.007, no heterogeneity)). However, meta-analysis with both fixed-effect and random-effects model on the data from the Beck Depression Inventory (mean difference with both models -1.57 (95% CL -4.30 to 1.16; P = 0.26, I(2) = 0) could not confirm the Hamilton Rating Scale for Depression results. Furthermore, trial sequential analysis on both the data from Hamilton Rating Scale for Depression and Becks Depression Inventory showed that insufficient data have been obtained.DiscussionCognitive therapy might not be an effective treatment for major depressive disorder compared with 'treatment as usual'. The possible treatment effect measured on the Hamilton Rating Scale for Depression is relatively small. More randomized trials with low risk of bias, increased sample sizes, and broader more clinically relevant outcomes are needed.
| S-EPMC3150380 | biostudies-literature
Project description:ObjectiveTo examine sexual functioning in adolescents with depression.MethodsBetween September 2010 and March 2014, 235 participants who were between 15 and 20 years old and were unmedicated or within 1 month of beginning antidepressant treatment completed the Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), and Changes in Sexual Functioning Questionnaire (CSFQ). They were also assessed to establish the presence of a DSM-IV-TR major depressive episode (MDE). The Student t test and χ² test were used to compare continuous and categorical variables, respectively, across participants with versus without MDE. Multivariable linear regression analysis examined the association between depression and sexual functioning.ResultsAfter the investigators controlled for age, female sex, antidepressant use, and the presence of generalized anxiety disorder, the presence of MDE was associated with a lower score on the CSFQ overall (P < .0007) and on its desire (P < .09), arousal (P < .001), and orgasm (P < .007) subscales. Antidepressants were not associated with sexual functioning either in the sample overall or in those with MDE. Beck Depression Inventory items related to affective symptoms (P < .03), rather than those tapping into neurovegetative or cognitive functioning, accounted for the association between depression and lower sexual functioning. Furthermore, with higher BDI scores, males exhibited a steeper decline than females in both the CSFQ total score and the desire subscale (sex × BDI score interaction effect: P < .03). Anxiety was not significantly associated with sexual functioning.ConclusionsMajor depressive disorder in older adolescents is associated with lower sexual functioning, particularly in males. This appears most related to affective symptoms. The potential impact of such impairment on future sexual functioning deserves further examination.Trial registrationClinicalTrials.gov identifier: NCT02147184.
| S-EPMC5520806 | biostudies-literature
Project description:Background: Cognitive dysfunction is considered a core feature among schizophrenia (SZ), bipolar disorder (BD), and major depressive disorder (MDD). Despite abundant literature comparing cognitive dysfunction among these disorders, the relationship between cognitive dysfunction and symptom dimensions remains unclear. The study aims are a) to identify the factor structure of the BPRS-18 and b) to examine the relationship between symptom domains and cognitive function across SZ, BD, and MDD. Methods: A total of 716 participants [262 with SZ, 104 with BD, 101 with MDD, and 249 healthy controls (HC)] were included in the study. One hundred eighty participants (59 with SZ, 23 with BD, 24 with MDD, and 74 HC) completed the MATRICS Consensus Cognitive Battery (MCCB), and 507 participants (85 with SZ, 89 with BD, 90 with MDD, and 243 HC) completed the Wisconsin Card Sorting Test (WCST). All patients completed the Brief Psychiatric Rating Scale (BPRS). Results: We identified five BPRS exploratory factor analysis (EFA) factors ("affective symptoms," "psychosis," "negative/disorganized symptoms," "activation," and "noncooperation") and found cognitive dysfunction in all of the participant groups with psychiatric disorders. Negative/disorganized symptoms were the most strongly associated with cognitive dysfunctions across SZ, BD, and MDD. Conclusions: Our findings suggest that cognitive dysfunction severity relates to the negative/disorganized symptom domain across SZ, BD, and MDD, and negative/disorganized symptoms may be an important target for effective cognitive remediation in SZ, BD, and MDD.
| S-EPMC6498739 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-08-08 | GSE214922 | GEO
Project description:Background: Major Depressive Disorder (MDD) is a moderately heritable disorder with a high lifetime prevalence. At present, laboratory blood tests to support MDD diagnosis are not available. Methods: We used a classifier approach on blood gene expression profiles of a unique set of non-medicated subjects (MDD patients and controls) to select genes of which expression is predictive for disease status. To reveal blood gene expression changes related to MDD disease, we applied a powerful ex vivo stimulus to the blood, i.e. incubation with lipopolysaccharide (LPS; 10 ng/ml blood). Results: Based on LPS-stimulated blood gene expression using whole-genome microarrays in 42 subjects (primary cohort; 21 MDD patients (mean age 42.3 years), 21 healthy controls (mean age 41.9 years)), we identified a set of genes (CAPRIN1, CLEC4A, KRT23, MLC1, PLSCR1, PROK2, ZBTB16) that serves as a molecular signature of MDD. These findings were validated for the primary cohort using an independent quantitative PCR method (P = 0.007). The difference between depressive patients and controls was confirmed (P = 0.019) in a replication cohort of 13 patients with MDD (mean age 42.8 years) and 14 controls (mean age 45.6 years). The MDD-signature score comprised of expression levels of 7 genes could discriminate depressive patients from controls with sensitivity of 76.9% and specificity of 71.8%. Conclusions: We show for the first time that molecular analysis of stimulated blood cells can be used as an endophenotype for MDD diagnosis, which is a milestone in establishing biomarkers for neuropsychiatric disorders with moderate heritability in general. Our results may provide a new entry point for following and predicting treatment outcome, as well as prediction of severity and recurrence of MDD. In total, 33 MDD patients and 34 healthy controls were analyzed using basal gene expression in whole blood, and gene expression from whole blood that was stimulated with LPS for 5-6 h, using microarrays. Patients were arbitrarily selected from all patients to serve as primary cohort (nMDD = 21 (MDD01-MDD21); nControls = 21 (Con01-Con21)), or replication cohort (nMDD = 12 (MDD22-MDD35); nControls = 13 (Con22-Con37)) using microarrays. This submission does not include Samples CON21_LPS or CON30_LPS.
2011-10-04 | E-GEOD-19738 | biostudies-arrayexpress
Project description:BackgroundAdults with major depressive disorder (MDD) demonstrate increased susceptibility to interfering effects of anxiety on cognitive control; although under certain conditions adults with MDD are able to compensate for these effects. The brain mechanisms that may facilitate the ability to compensate for anxiety either via the recruitment of additional cognitive resources or via the regulation of interference from anxiety remain largely unknown. To clarify these mechanisms, we examined the effects of anxiety on brain activity and amygdala-prefrontal functional connectivity in adults diagnosed with MDD.MethodA total of 22 unmedicated adults with MDD and 18 healthy controls (HCs) performed the Tower of London task under conditions designed to induce anxiety, while undergoing a functional magnetic resonance imaging assessment.ResultsDuring the easy condition, the MDD group demonstrated equivalent planning accuracy, longer planning times, elevated amygdala activity and left rostrolateral prefrontal cortex (RLPFC) hyperactivity relative to HCs. Anxiety mediated observed group differences in planning times, as well as differences in amygdala activation, which subsequently mediated observed differences in RLPFC activation. During the easy condition, the MDD group also demonstrated increased negative amygdala-dorsolateral prefrontal cortex (DLPFC) connectivity which correlated with improved planning accuracy. During the hard condition, HCs demonstrated greater DLPFC activation and stronger negative amygdala-DLPFC connectivity, which was unrelated to planning accuracy.ConclusionsOur results suggest that persons with MDD compensate for anxiety-related limbic activation during low-load cognitive tasks by recruiting additional RLPFC activation and through increased inhibitory amygdala-DLPFC communication. Targeting these neural mechanisms directly may improve cognitive functioning in MDD.
| S-EPMC4946974 | biostudies-literature