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Are Improvements in Cognitive Content and Depressive Symptoms Correlates or Mediators during Acute-Phase Cognitive Therapy for Recurrent Major Depressive Disorder?

ABSTRACT: The cognitive model of depression posits that cognitive therapy's (CT) effect on depressive symptoms is mediated by changes in cognitive content (e.g., automatic negative thoughts dysfunctional attitudes, failure attributions). We tested improvement and normalization of cognitive content among outpatients (N = 523) with recurrent major depressive disorder treated with acute-phase CT (Jarrett & Thase, 2010; Jarrett et al., 2013). We also tested whether improvement in cognitive content accounted for subsequent changes in depressive symptoms and vice versa. Five measures of content improved substantively from pre- to post-CT (median d = 0.96), and the proportions of patients scoring in "healthy" ranges increased (median 45% to 82%). Evidence for cognitive mediation of symptom reduction was limited (median r = .06), as was evidence for symptom mediation of cognitive content improvement (median r = .07). We discuss measurement and design issues relevant to detection of mediators and consider alternative theories of change.

SUBMITTER: Vittengl JR

PROVIDER: S-EPMC4577061 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature

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Are Improvements in Cognitive Content and Depressive Symptoms Correlates or Mediators during Acute-Phase Cognitive Therapy for Recurrent Major Depressive Disorder?

Vittengl Jeffrey R JR Clark Lee Anna LA Thase Michael E ME Jarrett Robin B RB

International journal of cognitive therapy 20140101 3

The cognitive model of depression posits that cognitive therapy's (CT) effect on depressive symptoms is mediated by changes in cognitive content (e.g., automatic negative thoughts dysfunctional attitudes, failure attributions). We tested improvement and normalization of cognitive content among outpatients (<i>N</i> = 523) with recurrent major depressive disorder treated with acute-phase CT (Jarrett & Thase, 2010; Jarrett et al., 2013). We also tested whether improvement in cognitive content acco ...[more]

PMID: 26401194

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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.

Project description:Imaging techniques are a potentially powerful method of identifying phenotypes that are associated with, or are indicative of, a vulnerability to developing major depressive disorder (MDD). Here we identify seven promising MDD-associated traits identified by magnetic resonance imaging (MRI) or positron emission tomography (PET). We evaluate whether these traits are state-independent, heritable endophenotypes, or state-dependent phenotypes that may be useful markers of treatment efficacy. In MDD, increased activity of the amygdala in response to negative stimuli appears to be a mood-congruent phenomenon, and is likely moderated by the 5-HT transporter gene (SLC6A4) promoter polymorphism (5-HTTLPR). Hippocampal volume loss is characteristic of elderly or chronically-ill samples and may be impacted by the val66met brain-derived neurotrophic factor (BDNF) gene variant and the 5-HTTLPR SLC6A4 polymorphism. White matter pathology is salient in elderly MDD cohorts but is associated with cerebrovascular disease, and is unlikely to be a useful marker of a latent MDD diathesis. Increased blood flow or metabolism of the subgenual anterior cingulate cortex (sgACC), together with gray matter volume loss in this region, is a well-replicated finding in MDD. An attenuation of the usual pattern of fronto-limbic connectivity, particularly a decreased temporal correlation in amygdala-anterior cingulate cortex (ACC) activity, is another MDD-associated trait. Concerning neuroreceptor PET imaging, decreased 5-HT(1A) binding potential in the raphe, medial temporal lobe, and medial prefrontal cortex (mPFC) has been strongly associated with MDD, and may be impacted by a functional single nucleotide polymorphism in the promoter region of the 5-HT(1A) gene (HTR1A: -1019 C/G; rs6295). Potentially indicative of inter-study variation in MDD etiology or mood state, both increased and decreased binding potential of the 5-HT transporter has been reported. Challenges facing the field include the problem of phenotypic and etiological heterogeneity, technological limitations, the confounding effects of medication, and non-disease related inter-individual variation in brain morphology and function. Further advances are likely as epigenetic, copy-number variant, gene-gene interaction, and genome-wide association (GWA) approaches are brought to bear on imaging data.

Project description:BackgroundMajor depressive disorder (MDD) is a common and burdensome condition. The clinical understanding of MDD is shaped by current research, which lacks insight into the patient perspective.ObjectiveThis two-part study aimed to generate data from PatientsLikeMe, an online patient network, on the perception of cognitive symptoms and their prioritization in MDD.MethodsA retrospective data analysis (study 1) was used to analyze data from the PatientsLikeMe community with self-reported MDD. Information on patient demographics, comorbidities, self-rated severity of MDD, treatment effectiveness, and specific symptoms of MDD was analyzed. A prospective electronic survey (study 2) was emailed to longstanding and recently active members of the PatientsLikeMe MDD community. Study 1 analysis informed the objectives of the study 2 survey, which were to determine symptom perception and prioritization, cognitive symptoms of MDD, residual symptoms, and medication effectiveness.ResultsIn study 1 (N=17,166), cognitive symptoms were frequently reported, including "severe" difficulty in concentrating (28%). Difficulty in concentrating was reported even among patients with no/mild depression (80%) and those who considered their treatment successful (17%). In study 2 (N=2525), 23% (118/508) of patients cited cognitive symptoms as a treatment priority. Cognitive symptoms correlated with depression severity, including difficulty in making decisions, concentrating, and thinking clearly (rs=0.32, 0.36, and 0.34, respectively). Cognitive symptoms interfered with meaningful relationships and daily life tasks and had a profound impact on patients' ability to work and recover from depression.ConclusionsPatients acknowledge that cognitive dysfunction in MDD limits their ability to recover fully and return to a normal level of social and occupational functioning. Further clinical understanding and characterization of MDD for symptom prioritization and relapse risk due to residual cognitive impairment are required to help patients return to normal cognitive function and aid their overall recovery.

Dataset Information

Are Improvements in Cognitive Content and Depressive Symptoms Correlates or Mediators during Acute-Phase Cognitive Therapy for Recurrent Major Depressive Disorder?

Publications

Are Improvements in Cognitive Content and Depressive Symptoms Correlates or Mediators during Acute-Phase Cognitive Therapy for Recurrent Major Depressive Disorder?

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