Cognitive Deficits In Depression Research Articles

Auditory P50 Sensory Gating Alterations in Major Depressive Disorder and their Relationship to Clinical Symptoms

Cognitive deficits in depression are pervasive and include impairments in attention and higher-order functions but the degree to which low-level sensory processes are affected is unclear. The present work examined event-related potential (P50 and N100) features of auditory sensory gating (i.e., the ability to inhibit P50/N100 responses to redundant stimuli) and their relationship to depressive symptoms, including ruminations and dysfunctional attitudes. In 18 patients with major depressive disorder (MDD) and 18 healthy volunteers, auditory sensory gating was measured using a paired-stimulus paradigm yielding ratio (rP50, rN100) and difference (dP50, dN100) gating indices, which reflected amplitude reductions from first (S1) to second (S2) stimulus. Patients with MDD exhibited diminished rP50 and dP50 gating scores and delayed S1-N100 latencies compared to healthy volunteers. These measures were positively associated with ruminative thoughts, negative attitudes and degree of depression. Study findings implicate aberrant sensory processing in depressed patients that is related to severity of maladaptive thinking.

“Don't [ruminate], be happy”: A cognitive perspective linking depression and anhedonia

Anhedonia, a lack of pleasure in things an individual once enjoyed, and rumination, the process of perseverative and repetitive attention to specific thoughts, are hallmark features of depression. Though these both contribute to the same debilitating disorder, they have often been studied independently and through different theoretical lenses (e.g., biological vs. cognitive). Cognitive theories and research on rumination have largely focused on understanding negative affect in depression with much less focus on the etiology and maintenance of anhedonia. In this paper, we argue that by examining the relation between cognitive constructs and deficits in positive affect, we may better understand anhedonia in depression thereby improving prevention and intervention efforts. We review the extant literature on cognitive deficits in depression and discuss how these dysfunctions may not only lead to sustained negative affect but, importantly, interfere with an ability to attend to social and environmental cues that could restore positive affect. Specifically, we discuss how rumination is associated to deficits in working memory and propose that these deficits in working memory may contribute to anhedonia in depression. We further argue that analytical approaches such as computational modeling are needed to study these questions and, finally, discuss implications for treatment.

Neural correlations between cognitive deficits and emotion regulation strategies: understanding emotion dysregulation in depression from the perspective of cognitive control and cognitive biases.

The link between cognitive function and emotion regulation may be helpful in better understanding the onset, maintenance, and treatment for depression. However, it remains unclear whether there are neural correlates between emotion dysregulation and cognitive deficits in depression. To address this question, we first review the neural representations of emotion dysregulation and cognitive deficits in depression (including deficits in cognitive control and cognitive biases). Based on the comparisons of neural representations of emotion dysregulation versus cognitive deficits, we propose an accessible and reasonable link between emotion dysregulation, cognitive control, and cognitive biases in depression. Specifically, cognitive control serves the whole process of emotion regulation, whereas cognitive biases are engaged in emotion regulation processes at different stages. Moreover, the abnormal implementation of different emotion regulation strategies in depression is consistently affected by cognitive control, which is involved in the dorsolateral, the dorsomedial prefrontal cortex, and the anterior cingulate cortex. Besides, the relationship between different emotion regulation strategies and cognitive biases in depression may be distinct: the orbitofrontal cortex contributes to the association between ineffective reappraisal and negative interpretation bias, while the subgenual prefrontal cortex and the posterior cingulate cortex underline the tendency of depressed individuals to ruminate and overly engage in self-referential bias. This review sheds light on the relationship between cognitive deficits and emotion dysregulation in depression and identifies directions in need of future attention.

Depression and Cognitive Impairment: Current Understanding of Its Neurobiology and Diagnosis.

Eye movement is critical for obtaining precise visual information and providing sensorimotor processes and advanced cognitive functions to the brain behavioral indicator. In this article, we present a narrative review of the eye-movement paradigms (such as fixation, smooth pursuit eye movements, and memory-guided saccade tasks) in major depression. Characteristics of eye movement are considered to reflect several aspects of cognitive deficits regarded as an aid to diagnosis. Findings regarding depressive disorders showed differences from the healthy population in paradigms, the characteristics of eye movement may reflect cognitive deficits in depression. Neuroimaging studies have demonstrated the effectiveness of different eye movement paradigms for MDD screening. Depression can be distinguished from other mental illnesses based on eye movements. Eye movement reflects cognitive deficits that can help diagnose depression, and it can make the entire diagnostic process more accurate.

The effectiveness of computerized cognitive remediation therapy (CCRT) for deficits in attention and executive functions in depression: A pilot study

Depression is associated with cognitive deficits and changes in the brain. Major depression is often associated with cognitive problems; however, there are only a few studies that have focused on the systematic use of cognitive remediation in depression. The objective of this study was to assess the effectiveness of computerized cognitive remediation in depressed patients with cognitive dysfunction. Patients (n = 20) with depression were randomly assigned to the active or control group. The active intervention (computerized cognitive remediation) comprised 12 sessions focused on the remediation of attention and executive functions through the CogniPlus software. All participants completed neuropsychological testing before and after the intervention. A mixed-design analysis of variance revealed a significant time × group interaction in the attention and planning task, on the Beck Depression Inventory and on the Shifting, Emotional Control and Initiating sub-scales of the Behavior Rating Inventory of Executive Function-Adult. The results showed that patients undergoing cognitive remediation improved in domains related to attention and executive functions and scored significantly lower on the Beck Depression Inventory. The findings provide some evidence that cognitive remediation could be an efficient approach to dealing with cognitive deficits in depression.

Geriatric Depression and Cognitive Impairment-An Update.

Background:Depression and cognitive impairment often coexist in older adults. The relation between depression and cognitive impairment is complex. The objective of this article is to review recent literature on cognitive impairment in older adults with depression and provide clinicians an update.Methods:We searched PubMed, Google Scholar, Science Direct, and Psych Info for the articles published in the English language related to late-life depression (LLD)/geriatric depression and cognitive impairment. We considered original research articles, relevant systematic reviews, chapters, and important conceptual articles published in the last 9 years (2011–2019). We selected relevant articles for this narrative review.Conclusion:The concept pseudodementia, indicating depression with cognitive impairment mimicking dementia, is now seen only as a historical concept. The current literature strongly agrees with fact that cognitive deficits often exist in LLD. The cognitive deficits in depression were initially seen as trait marker; however, some recent studies suggest that cognitive deficits persist even in the remission phase. There is heterogeneity among the studies in terms of the nature of the cognitive deficits, but higher number of studies reported impairment in attention and executive function. LLD with cognitive deficits is at a higher risk of progression to dementia. In older adults, depression with cognitive impairments requires a comprehensive evaluation. Electroencephalography, event-related potentials, fluorodeoxyglucose–positron emission tomography, amyloid positron emission tomography, and CSF amyloid will supplement clinical evaluation in differentiating functional depressive disorder with cognitive impairment from depression with an underlying degenerative condition.

Higher inflammation and cerebral white matter injury associated with cognitive deficit in asthmatic patients with depression

Objective Depression is a common co-morbidity in asthma, worsening asthma control and impairing quality of life. Previous studies have reported a higher risk of cognitive deficit in depression, yet little research has focused on the level of cognition in asthmatic patients with depression. Evidence shows that inflammation may play an important role in both asthma and depression. Cerebral white matter injury, possibly induced by inflammation, has been associated with depression. This study assesses cognitive function in patients with asthma and a depression comorbidity, compared to patients with asthma only or depression only. Methods Four groups were studied: Asthma comorbid Depression group (A + D, n = 26), Depression group (D, n = 25), Asthma group (A, n = 33) and Normal controls (N, n = 28). Cognitive function was evaluated using Montreal Cognitive Assessment (MoCA). Inflammatory cytokines were measured, including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), high-mobility group box 1(HMGB1) and Netrin-1. Cerebral white matter injury was assessed by serum myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG), and their correlations with cognitive performance were calculated. Results A + D group showed the highest incidence of cognitive deficit, with the cognitive domain particularly affected. Compared to N group, serum levels of IL-6, HMGB1, Netrin-1, MBP and MOG were significantly elevated in A + D group. MOG level negatively correlated with the MoCA score. Conclusion Patients with comorbidities presented with more severe cognitive deficits and higher levels of inflammatory cytokines. Cerebral white matter injury may account for the cognitive deficit in patients and MOG could be a potential biomarker for this process.

Study of neuropsychological deficits in late onset depression.

Older adults with depression often have cognitive deficits contributing to higher morbidity and increased risk for conversion to dementia. Research on this area is limited from India. The objective of the current study is to examine the neuropsychological measures in older adults with Late-onset depression (LOD) compared to healthy controls (HC). Sample included older adults with depression as per DSM-IV TR criteria seeking treatment from Geriatric Clinic and Services, National Institute of Mental Health and Neurosciences (NIMHANS). Geriatric depression scale, Montgomery Asberg depression rating scale and Hamilton anxiety rating scale were applied to screen and measure the severity of depression. Comprehensive assessment of neurocognitive function was done using NIMAHNS Neuropsychological Battery for Elderly (NNBE, 2013). Sample included 76 LOD patients and 76 healthy controls (HC) who were matched for age, gender and education. The mean age of onset of illness was 63.17(SD-6.54) years and median duration of total illness was 29.5 months. In the standard assessments, the mean score on GDS was 9.28 (SD-3.32) and MADRS was 18.88 (SD-6.07). The LOD group had lower Hindi Mental Status Examination (HMSE) score compared to HC (28.64 ± 2.09 vs 30.05 ± 1.26, p < 0.001). Compared to HC, LOD group performed poorly on tasks of attention, executive function, verbal and visual memory, verbal fluency and visuo-spatial skills. Recognition memory and logical memory were relatively preserved in LOD compared to HC. Cognitive deficits were seen predominantly in attention and executive function, visuo-spatial skills and memory similar to previous studies. It is advisable to routinely assess cognitive symptoms in older adults presenting with depression.

Alleviation of cognitive deficits and high copper levels by an NMDA receptor antagonist in a rat depression model

BackgroundMajor depressive disorder (MDD) is frequently associated with cognitive deficits and high copper levels. Dysfunction of N-methyl-d-aspartate (NMDA) receptors has been postulated to underlie MDD pathogenesis. This study sought to investigate the curative effect of the NMDA receptor antagonist memantine on cognitive deficits in depression and the underlying mechanisms. MethodsAdult male Sprague-Dawley rats received corticosterone (CORT) (20 mg/kg) bi-weekly via subcutaneous injection and/or copper gluconate (7 mg/kg) via daily intragastric administration. After 3 weeks, sucrose preference tests and open field tests showed anhedonia and high anxiety in both the CORT and CORT+Cu groups. Memantine intervention (20 mg/kg daily via intragastric administration for 14 days) led to recovery of anhedonia and anxiety behaviors. Memantine also remarkably suppressed serum copper ion levels. Moreover, memantine treatment effectively rescued depression-related spatial memory deficits as shown by the Morris water maze task. ResultsCompared to the pre-memantine treatment results, the results of behavioral tests and cognitive function after memantine treatment were significantly normalized, and the copper concentration was decreased in all groups. ConclusionsCollectively, our findings suggest that the NMDA receptor antagonist memantine may improve symptoms of anhedonia and anxiety and the cognitive deficits associated with depression, likely be related to suppress serum copper ion levels.

N-acetyl cysteine ameliorates depression-induced cognitive deficits by restoring the volumes of hippocampal subfields and associated neurochemical changes

Depression is highly comorbid with anxiety disorders and associated with profound cognitive impairment. Moreover, cognitive deficits associated with hippocampal dysfunction are central in depression and anxiety disorders. Furthermore, depression is accompanied by glutamatergic dysfunction which can further impair the functioning of the hippocampus. Recent studies have shown that N-acetyl cysteine (NAC), a glutamate modulator produces an antidepressant-like effect by normalization of the periterminal release of glutamate and/or antioxidant effects. However, the effects of repeated NAC treatment on depression-induced anxiety, cognitive deficits, and associated neurochemical and structural alterations are relatively unknown. Accordingly, we investigated whether chronic NAC treatment could reverse cognitive deficits, and associated hippocampal volume loss and monoaminergic alterations in the neonatal clomipramine (CLI) model of depression. We found that chronic NAC treatment produces antidepressive and antianhedonic-like effects. NAC treatment also reversed CLI-induced anxiety. Interestingly, repeated NAC treatment improved the performance of CLI rats in rewarded alternation task in T-maze. The antidepressive-like and procognitive effects of NAC was associated with normalization of volume loss in CA1, dentate gyrus (DG) and hilar subfields of the hippocampus. Furthermore, NAC restored CLI-induced decrease in levels of monoamines and normalized enhanced metabolism in the hippocampus. Taken together, chronic NAC treatment ameliorates depressive and anxiety-like behavior, spatial learning deficits, and reverses CLI-induced pathological alterations at structural and neurochemical levels in the hippocampus. Our findings might help in evolving NAC as a viable pharmacotherapy for reversal of cognitive deficits in depression and associated disorders.

Pharmacological treatment of cognitive deficits in nondementing mental health disorders .

Evidence for pharmacological remediation of cognitive deficits in three major psychiatric disorders—attention deficit- hyperactivity disorder (ADHD), schizophrenia, and depression—is reviewed. ADHD is effectively treated with the stimulant medications methylphenidate and d-amphetamine, as well as nonstimulants such as atomoxetine, implicating cognitive enhancing effects mediated by noradrenaline and dopamine. However, the precise mechanisms underlying these effects remains unclear. Cognitive deficits in schizophrenia are less effectively treated, but attempts via a variety of neurotransmitter strategies are surveyed. The possibility of treating cognitive deficits in depression via antidepressant medication (eg, selective serotonin reuptake inhibitors) and by adjunctive drug treatment has only recently received attention because of confounding, or possibly interactive, effects on mood. Prospects for future advances in this important area may need to take into account transdiagnostic perspectives on cognition (including neurodegenerative diseases) as well as improvements in neuropsychological, neurobiological, and clinical trial design approaches to cognitive enhancement.

Early shifts of emotional attention as a possible predictor of remission in patients with depression receiving ECT: Preliminary results of an eye-tracker study

Background Electro-convulsive therapy (ECT) is one of the most effective treatment for treatment resistant depression (TRD) with remission rates of 87% [1] . Despite such a significant clinical effect generally observed after 6 to 20 sessions, ECT is also accompanied by major cognitive side effects and no markers of remission are available to help practitioners deciding to continue or not to deliver ECT sessions. Evidence suggests that early improvements in emotional processing, a commonly observed cognitive deficits in depression, can predict later clinical response to antidepressant [2] . Based on these studies, we hypothesized that early enhancement in emotional processing would predict remission in patients receiving ECT. Methods In an open pilot study, 30 patients with TRD receiving ECT will be enrolled. A free-viewing eye-tracking paradigm will be used to measure preferential attention to positive, negative or neutral faces. In this task patients will have to passively watch 2 pictures of faces (one neutral and one emotional face) presented during 3.5 sec on a computer screen. Eye-gaze patterns and time spend to the affective and to the neutral face will be assessed twice, one time at baseline and one time after the 6th ECT session. Severity of depression will be assessed using the MADRS at baseline, after the 6th and after the last ECT sessions. Results We report preliminary results in 8 patients. At the 6th ECT session, attention to happy faces was improved by 27% after 6 ECT treatments as compared to baseline in future remitters (MADRS Conclusion Early modification at free-viewing eye-tracking paradigm measuring emotional attention could be a predictive marker of remission to ECT in patients with TRD. Further investigation are needed to confirm this hypothesis.

Abnormal coupling among spontaneous brain activity metrics and cognitive deficits in major depressive disorder

BackgroundA variety of functional metrics derived from resting-state functional magnetic resonance imaging (rs-fMRI) have been employed to explore spontaneous brain activity changes in major depressive disorder (MDD) and have enjoyed significant success in unraveling the neurobiological mechanisms underlying this disorder. However, it is unclear whether spatial and temporal coupling relationships among these rs-fMRI metrics are altered in MDD. Methods50 patients with MDD and 36 well-matched healthy controls underwent rs-fMRI scans. A dynamic analysis was applied to compute multiple frequently used metrics including fractional amplitude of low frequency fluctuations, regional homogeneity, voxel-mirrored homotopic connectivity, degree centrality and global signal connectivity. Kendall's W was used to calculate volume-wise (across voxels) and voxel-wise (across time windows) concordance among these metrics. Inter-group differences in the concordance and their associations with clinical and cognitive variables were tested. ResultsCompared to healthy controls, patients with MDD showed decreased whole gray matter volume-wise concordance. Despite similar spatial distributions, quantitative comparison analysis revealed that MDD patients exhibited reduced voxel-wise concordance in multiple cortical and subcortical regions. Moreover, the lower concordance was associated with worse performances in prospective memory and sustained attention in the MDD group. LimitationsThe study design of fairly modest sample size did not allow us to perform a full analysis of the potential effects of medication and illness duration. ConclusionsOur findings suggest that spatial and temporal decoupling of multiple resting-state brain activity metrics may help elucidate the neural mechanisms of cognitive deficits in depression.

A systematic review of the impact of social cognitive deficits on psychosocial functioning in major depressive disorder and opportunities for therapeutic intervention

Social cognition is the ability to identify, perceive and interpret socially relevant information from the external world. It is an important adaptive trait, but is frequently affected in major depressive disorder by a mood-congruent interpretive bias. The present review examined the existing body of literature to determine (i) the impact social cognitive deficits in depression have on psychosocial functioning; and (ii) the utility of psychotropic, psychological and procedural interventions employed to target these deficits. A total of 107 studies met inclusion criteria for review. Social cognitive performance was found to adversely impact depressed patients’ psychosocial functioning across the key domains of general cognitive functioning and quality of life. Secondly, many current therapies were found to have a normalising effect on the social cognitive abilities of subjects with major depressive disorder, both at a neural and functional level. In particular, certain anti-depressant medications corrected facial affect recognition deficits, while several psychotherapeutic approaches improved impairments in theory of mind and negative interpretive bias.

The relationship between social cognition and executive function in Major Depressive Disorder in high-functioning adolescents and young adults

To understand how cognitive dysfunction contributes to social cognitive deficits in depression, we investigated the relationship between executive function and social cognitive performance in adolescents and young adults during current and remitted depression, compared to healthy controls. Social cognition and executive function were measured in 179 students (61 healthy controls and 118 patients with depression; Mage = 20.60 years; SDage = 3.82 years). Hierarchical regression models were employed within each group (healthy controls, remitted depression, current depression) to examine the nature of associations between cognitive measures. Social cognitive and executive function did not significantly differ overall between depressed patients and healthy controls. There was no association between executive function and social cognitive function in healthy controls or in remitted patients. However, in patients with a current state of depression, lower cognitive flexibility was associated with lower performance in facial-affect recognition, theory-of-mind tasks and overall affect recognition. In this group, better planning abilities were associated with decreased performance in facial affect recognition and overall social cognitive performance. While we infer that less cognitive flexibility might lead to a more rigid interpretation of ambiguous social stimuli, we interpret the counterintuitive negative correlation of planning ability and social cognition as a compensatory mechanism.

Dopaminergic mechanisms in memory consolidation and antidepressant reversal of a chronic mild stress-induced cognitive impairment`

Cognitive deficits in depression can be modelled using the novel object recognition (NOR) test, performance in which is impaired by chronic mild stress (CMS). We aimed to examine the involvement of mesocorticolimbic DA terminal regions, and to establish the substrate for CMS-induced impairment of NOR and its reversal by chronic antidepressant treatment. In experiments 1 and 2, we examined the effect of infusions into medial PFC, dorsal hippocampus (HPC), and nucleus accumbens (NAc) shell of D1 and D2 antagonists and D3 agonist, which were predicted to impair NOR with a short (1 h) delay, and of D1 and D2 agonists and D3 antagonist, which were predicted to facilitate NOR with a long (24 h) delay. Using optimal doses identified in experiment 2, in experiments 3 and 4, we examined effects on drug-stimulated NOR of CMS and chronic treatment with venlafaxine (VFX) or risperidone (RSP). We found a wide involvement of DA systems in memory for NOR: D1 receptors in PFC, HPC, and NAc; D3 receptors in PFC and HPC; and D2 receptors in PFC. CMS impaired D2- and D3-mediated effects in PFC and HPC; antidepressants rescued those effects in PFC but not HPC. The involvement of DA in NOR is multifaceted, but the effects of CMS and antidepressants are more discrete, involving D2 and D3 receptors in PFC specifically. While raising many difficult questions, these results suggest that the D2 and D3 receptors in the medial PFC may be an important substrate for cognitive deficits in depression and their remediation.

Vortioxetine reduces BOLD signal during performance of the N-back working memory task: a randomised neuroimaging trial in remitted depressed patients and healthy controls

Cognitive dysfunction is common in depression during both acute episodes and remission. Vortioxetine is a novel multimodal antidepressant that has improved cognitive function including executive function in depressed patients in randomised placebo-controlled clinical trials. However, it is unclear whether vortioxetine is able to target directly the neural circuitry implicated in the cognitive deficits in depression. Remitted depressed (n=48) and healthy volunteers (n=48) were randomised to receive 14 days treatment with 20 mg vortioxetine or placebo in a double-blind design. The effects of treatment on functional magnetic resonance imaging responses during an N-back working memory task were assessed at baseline and at the end of treatment. Neuropsychological measures of executive function, speed and information processing, attention and learning and memory were examined with the Trail Making Test (TMT), Rey Auditory Learning Test and Digit Symbol Substitution Test before and after treatment; subjective cognitive function was assessed using the Perceived Deficits Questionnaire (PDQ). Compared with placebo, vortioxetine reduced activation in the right dorsolateral prefrontal cortex and left hippocampus during the N-back task compared with placebo. Vortioxetine also increased TMT-A performance and self-reported cognitive function on the PDQ. These effects were seen across both subject groups. Vortioxetine modulates neural responses across a circuit subserving working memory in a direction opposite to the changes described in depression, when performance is maintained. This study provides evidence that vortioxetine has direct effects on the neural circuitry supporting cognitive function that can be dissociated from its effects on the mood symptoms of depression.

Cognitive performance in unipolar old-age depression: a longitudinal study.

Previous studies on cognitive deficits in acute and remitted states of old-age depression have shown mixed findings. The episodic nature of depression makes repeated assessment of cognitive performance important in order to address reversibility and stability of cognitive deficits. Dementia-free older participants (≥60 years) from the population-based Swedish National Study on Aging and Care in Kungsholmen who completed neuropsychological testing at baseline (T1) and follow-up (T2) formed the basis of the study sample. Participants were grouped according to depression status at T1 and T2: depressed-remitted (n = 32), remitted-depressed (n = 45), and nondepressed-depressed (n = 29). These groups were compared with a group of randomly selected and matched (age, gender, education, and follow-up time) healthy controls (n = 106) over a period of maximum 6 years. Mixed ANCOVAs, controlling for age and gender, revealed depression-related deficits for processing speed, attention, executive function, and category fluency. In remitted states, only processing speed and attention were affected. However, these deficits were attenuated after exclusion of persons using benzodiazepine medications. A general pattern of cognitive decline was observed across all groups for processing speed, executive function, category fluency, and episodic and semantic memory; persons transitioning from a nondepressed to depressed state tended to show exacerbated cognitive decline. The results support the notion that cognitive deficits in depression may be more transient than stable. Consequently, cognitive deficits in depression might be regarded as potential treatment targets rather than stable vulnerabilities. As such, repeated assessment of cognitive functioning may provide an additional marker of treatment response.

Behavioral Evidence for an Impairment of Affective Theory of Mind Capabilities in Chronic Depression

Background: The only treatment specifically developed for chronic depression, the Cognitive Behavioral Analysis System of Psychotherapy (CBASP), is based amongst others on the hypothesis that chronically depressed patients (CD) show considerable deficits of affective theory of mind (ToM) capabilities. Data are scarce, however, and it remains unclear if ToM deficits are specific or if they arise from global cognitive deficits associated with depression. This study investigates the specific deficits of affective ToM abilities in CD. Sampling and Methods: ToM abilities were assessed in 26 medication-free CD and 26 matched healthy controls (HC) by means of a previously established false-belief ToM cartoon task. Since the task allowed an intern control for cognitive factors - operationalized in a visuospatial ToM task - it was possible to investigate specific affective ToM deficits. Results: As hypothesized, the CD showed a significant specific slowdown of affective ToM compared to cognitive ToM (3rd person perspective) when compared to HC. Simultaneously, we observed a general deterioration of all ToM functions in CD. Conclusions: This study provides evidence that CD have a mentalization deficit, specifically for affective ToM functions. This deficit is combined with a general deterioration of ToM functions, most likely attributable to frequently described cognitive deficits in depression.

The enduring effects of depressive thoughts on working memory

BackgroundDepressive thoughts are known to persist in persons with depressed mood leading to rumination and exacerbation of depressive symptoms. What has not yet been examined is whether this persistence of depressive thoughts can lead to impairment of working memory (WM). MethodsWe assessed whether receiving a WM task featuring depressive cues could bias performance on a subsequent, non-depressive WM task for dysphoric individuals (DIs) compared to non-DIs. ResultsDIs showed significantly attenuated performance on the WM task with depressive cues compared to non-DIs. Further, when DIs were given the WM task with depressive cues first, they showed deficits on a second WM task without depressive cues, compared to DIs given the non-depressive WM task first and non-DIs in either condition. LimitationsUnselected recruitment procedures did not permit balanced sample sizes in each group. Future research is needed to assess whether these results extend to a clinically depressed sample and whether WM deficits are the consequence of depressed mood, or a risk factor for the development and maintenance of depressed mood. ConclusionsResults suggest that, for DIs, the influence of depressive cues on performance transfers to subsequent tasks in which these cues are no longer present. These results support the hypothesis that when depressive thoughts are part of depressed persons’ conscious experience, cognitive deficits arise. Further, these results suggest an ecologically-relevant mechanism by which day-to-day cognitive deficits in depression can develop.