Depressive Cognitive Impairment Research Articles

Association of MicroRNA-146a-5p Polymorphism with Cognitive Impairment in Adolescents with Depressive Disorder

Introduction: The incidence of depression in adolescents is increasing and is associated with severe cognitive impairment. This paper aimed to investigate the relationship between polymorphisms in microRNA-146a-5p (miR-146a-5p) and cognitive impairment in adolescent depression patients. Methods: Quantitative real-time polymerase chain reaction was used to quantify miR-146a-5p in serum. Detection of miR-146a-5p gene polymorphism was performed by TaqMan SNP Genotyping Assay. Odds ratios and 95% confidence intervals (CIs) were calculated by chi-square test (χ2) and logistic regression analysis. Results: Genotyping of miR-146a rs2910164 showed that CC (OR = 0.443, 95% CI, 0.264–0.741, p = 0.002) and GC (OR = 0.445, 95% CI, 0.279–0.712, p = 0.001) genotype reduced the risk of cognitive impairment in adolescent depression. The C allele (OR = 0.794, 95% CI, 0.694–0.741, p = 0.001) was a protective factor for cognitive impairment in adolescent depression compared to the rs2910164 G allele. Rs2910164 (OR = 0.425, 95% CI = 0.273–0.662, p = 0.000) showed a negative correlation with adolescents with cognitive impairment in depression by logistic regression analysis. The level of miR-146a-5p was decreased in carriers of the CC and CG genotypes. Conclusion: Rs2910164 C allele carriers have a low risk of cognitive impairment in adolescent depression and could reduce miR-146a-5p level.

Reviving Bistable Perception in Patients With Depression by Decreasing the Overestimation of Prior Precision.

Slower perceptual alternations, a notable perceptual effect observed in psychiatric disorders, can be alleviated by antidepressant therapies that affect serotonin levels in the brain. While these phenomena have been well documented, the underlying neurocognitive mechanisms remain to be elucidated. Our study bridges this gap by employing a computational cognitive approach within a Bayesian predictive coding framework to explore these mechanisms in depression. We fitted a prediction error (PE) model to behavioral data from a binocular rivalry task, uncovering that significantly higher initial prior precision and lower PE led to a slower switch rate in patients with depression. Furthermore, serotonin-targeting antidepressant treatments significantly decreased the prior precision and increased PE, both of which were predictive of improvements in the perceptual alternation rate of depression patients. These findings indicated that the substantially slower perception switch rate in patients with depression was caused by the greater reliance on top-down priors and that serotonin treatment's efficacy was in its recalibration of these priors and enhancement of PE. Our study not only elucidates the cognitive underpinnings of depression, but also suggests computational modeling as a potent tool for integrating cognitive science with clinical psychology, advancing our understanding and treatment of cognitive impairments in depression.

Not Just a Mood Disorder─Is Depression a Neurodevelopmental, Cognitive Disorder? Focus on Prefronto-Thalamic Circuits.

Depression is one of the most burdensome psychiatric disorders, affecting hundreds of millions of people worldwide. The disease is characterized not only by severe emotional and affective impairments, but also by disturbed vegetative and cognitive functions. Although many candidate mechanisms have been proposed to cause the disease, the pathophysiology of cognitive impairments in depression remains unclear. In this article, we aim to assess the link between cognitive alterations in depression and possible developmental changes in neuronal circuit wiring during critical periods of susceptibility. We review the existing literature and propose a role of serotonin signaling during development in shaping the functional states of prefrontal neuronal circuits and prefronto-thalamic loops. We discuss how early life insults affecting the serotonergic system could be important in the alterations of these local and long-range circuits, thus favoring the emergence of neurodevelopmental disorders, such as depression.

Synapse-Related Serum and P300 Biomarkers Predict the Occurrence of Mild Cognitive Impairment in Depression.

Cognitive impairment is one of the common concomitant symptoms of depression. The aims of the present study were to predict the occurrence of mild cognitive impairment (MCI) in patients with depression. In this study, 217 patients with depression were recruited. Demographic data, serum indices and ERP indices from all participants were collected in the baseline period. The participants were followed for one year, and data from 200 patients were included in final analysis. Patients with depression were divided into those with MCI group (DWM group; n=145) and those without MCI (DWOM group; n=55). Data from the DWM group and the DWOM group were used to construct a logistic regression model, and a receiver operating characteristic (ROC) curve was drawn. Another 72 patients were used to validate the accuracy of our model. Compared with DWOM individuals, DWM individuals were more likely to live alone (P<0.05), had lower baseline serum levels of brain-derived neurotrophic factor (BDNF), fibroblast growth factor 2 (FGF2), and fibroblast growth factor 22 (FGF22) (P<0.05), and exhibited higher baseline latencies of P300, mismatch negativity (MMN), and N200 (P<0.05). Baseline serum BDNF and FGF22 levels, along with the P300 latency, were selected to construct the regression model using logistic regression. The regression equation was [Formula: see text], and the combination of the 3 indices yielded an area under the ROC curve (AUC) of 0.790 and a predictive accuracy of 0.806. The logistic regression model and ROC curves based on serum BDNF and FGF22 levels and the P300 latency could provide a more effective means to predict the occurrence of MCI in patients with depression.

Quercetin Ameliorates Cognitive Impairment in Depression by Targeting HSP90 to Inhibit NLRP3 Inflammasome Activation.

Cognitive dysfunction was a common symptom of major depressive disorder (MDD). In previous studies, psychological stress leads to activation and proliferation of microglial cells in different brain regions. Quercetin, a bioflavonoid derived from vegetables and fruits, exerts anti-inflammatory effects in various diseases. To demonstrate the role of quercetin in thehippocampal inflammatory response in depress mice. The chronic unpredictable stress (CUS) depressive mice model built is used to explore the protective effects of quercetin on depression. Neurobehavioral test, protein expression of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) and heat shock protein 90 (HSP90), and cytokines (IL-6, IL-1β, MCP-1, and TNF-α) were assessed. Quercetin ameliorated depressive-like behavior and cognitive impairment, and quercetin attenuates neuroinflammation and by targeting HSP90 to inhibit NLRP3 inflammasome activation. Quercetin inhibited the increase of HSP90 levels in the hippocampus and reverses inflammation-induced cognitive impairment. Besides, quercetin inhibited the increased level of cytokines (IL-6, IL-1β, MCP-1, and TNF-α) in the hippocampus of the depressive model mouse and the increased level of cytokines (IL-6, IL-1β, and MCP-1) in microglia. The current study indicated that quercetin mitigated depressive-like behavior and by targeting HSP90 to inhibit NLRP3 inflammasome activation in microglia and depressive mice model, meanwhile ameliorated cognitive impairment in depression. Quercetin has huge potential for the novel pharmacological efficacy of antidepressant therapy.

The functional role of the pulvinar in discriminating between objective and subjective cognitive impairment in major depressive disorder.

Emotionally driven cognitive complaints represent a major diagnostic challenge for clinicians and indicate the importance of objective confirmation of the accuracy of depressive patients' descriptions of their cognitive symptoms. We compared cognitive status and structural and functional brain connectivity changes in the pulvinar and hippocampus between patients with total depression and healthy controls. The depressive group was also classified as "amnestic" or "nonamnestic," based on the members' subjective reports concerning their forgetfulness. We then sought to determine whether these patients would differ in terms of objective neuroimaging and cognitive findings. The right pulvinar exhibited altered connectivity in individuals with depression with objective cognitive impairment, a finding which was not apparent in depressive patients with subjective cognitive impairment. The pulvinar may play a role in depression-related cognitive impairments. Connectivity network changes may differ between objective and subjective cognitive impairment in depression and may play a role in the increased risk of dementia in patients with depression.

Cognitive impairment and depression

The commonality of cognitive impairment and depression is discussed. Cognitive symptoms are the main symptoms of depressive disorder and, most often, it is cognitive impairment that reduces the performance and quality of life of depressed patients. The most common cognitive disorders in depressed patients are: attention deficit (both visual and auditory), decrease in the level of short-term and operative memory, difficulties in processing information of any modality, a decrease in the speed of information processing, as well as difficulties in building an activity program and monitoring her execution. A cognitive symptom that requires further discussion is the so-called cognitive distortion – a shift in focus from positive to negative stimuli, as well as incorrect reactions to negative feedback and decision making. A depressive episode develops against the background of dysmetabolic and dysfunctional cerebral changes in the amygdala, cingulate cortex, hippocampus, orbitofrontal and mediobasal frontal cortex. Cognitive impairment in patients who have had depression persists after recovery from depression; according to the figurative expression adopted in the scientific community of specialists studying cognitive impairment in depression, each depressive episode forms permanent “cognitive scars”. Presumably, cognitive dysfunction may be one of the risk factors for the development of a depressive disorder; depression, in turn, is a risk factor for the development of dementia, including in Alzheimer’s disease and cerebrovascular disease: studies have shown that the transformation of severe cognitive impairment associated with depression into dementia in elderly patients can reach 70% in five years. The undoubted commonality of depression and cognitive dysfunction is emphasized by the frequency of depression in patients with cognitive impairment.

Cognitive deficits in depressive disorder

Depression is a globally prevalent mental disorder, often accompanied by various cognitive impairments. Cognitive impairment in depression is related to brain dysfunction, resulting from focal brain damage affecting cognitive functions. Its primary manifestations include memory loss, visual disturbances, hallucinations, executive function deficits, and difficulties in sustaining attention. Cognitive functions encompass perception, cognition, and interaction with the external environment, constituting complex brain processes. Presently, our understanding of cognitive impairment in depression remains somewhat limited, underscoring the importance of further in-depth research. Damage to specific brain regions such as the amygdala, hippocampus, and medial temporal lobe can result in cognitive deficits in severe depression patients. Interventions tailored to these lesions, such as computerized cognitive tasks and brain stimulation techniques, contribute to cognitive improvement in depression patients. Cognitive-behavioral therapy and relaxation techniques, including breath control, assist patients in reducing stress and negative emotions. Cognitive bias modification and creative art therapy promote both mental and physical well-being. Moreover, exposure to pleasant music and engaging in aerobic exercise facilitate the recovery of depression patients with cognitive impairments. Regarding pharmacological treatments, duloxetine, vortioxetine, liraglutide, intranasal insulin, and intracerebral insulin can be employed for intervention in cognitive impairment associated with depression.

60 Recognition of Emotional Words: Relationship Between Rumination, Depression, Objective and Subjective Cognitive Impairment

Objective:Cognitive impairment in depression could present as subjective and objective, but the intensity of subjective impairment is higher and is not correlated with the deficits measured by neuropsychological tests. Subjective cognitive impairment lowers quality of life and is associated with the severity of depression. Among depressive patients, negative emotional bias is present. It is better memory for negative or positive information than for neutral information. We hypothesized that rumination is associated with subjective cognitive impairment.Participants and Methods:The study was performed through the online PsyToolkit platform. The study sample consisted of 168 healthy controls and 93 patients with depression were enrolled in the study. Participants completed questionnaires and performed a memory task that contained emotional words. The forty words were chosen from the Nencki Affective Word List. The list for memory test consists of 5 words from each Category: Happiness, Anger, Fear, Sad, Disgusting, and Neutral, and 10 words from category ‘Unclassified’ to balance the valence and arousal of the set. After 15 minutes, they recognized old words from the list of 80 words. Half of them were the same as in the first part, and other words were new, chosen with the same criteria. Depression symptoms were measured using the Beck Depression Inventory-II, subjective cognitive impairment with the Perceived Deficits Questionnaire-20, and intensity of rumination with the Polish Questionnaire of Rumination.Results:Subjective cognitive impairment and rumination were higher in patients with depression. They also had a higher error rate than healthy controls U = 6462.5; p = .021, especially in words from the neutral (U = 6292; p = .008) and happiness category (U = 6585; p = .031). However, there was no association between subjective cognitive impairment and performance in memory tasks. The regression analysis showed that depressive symptoms and intensity of rumination are better predictors of subjective cognitive deficits than objective performance on a memory task. The results of PDQ-20 were correlated with the error rate of words from categories: Happiness (r = -.162**), Sad (r = -.116*) and Neutral (r = -.145**). Words from categories Happiness, Disgust and Neutral were significantly better recognized than Unclassified, Fear or Sad group of words χ 2 F (6) = 132.685; p &lt; .001. In MDD group recognition of Disgust words were statistically highest than Anger and Fear words χ 2 F (6) = 36.795; p &lt; .001. The recognition of Happiness and Neutral word were not significantly different to other words.Conclusions:Cognitive problems are common in depression and affect quality of life. Subjective cognitive impairment is more closely related to rumination than objective cognitive impairment among healthy participants and patients with major depressive disorder. Emotional bias among depressive patients has been partially confirmed. Emotional impact is important for memory of words and subjective perception of cognition.

Autonomic dysregulation, cognition and fatigue in people with depression and in active and healthy controls: observational cohort study

Background Autonomic nervous system (ANS) dysregulation might be relevant to the pathophysiology of fatigue and cognitive impairment in depression and perhaps should be considered when making prescribing decisions. Aims To determine the relationship of self-reported ANS symptoms with fatigue, cognition and prescribed medication in people with a diagnosis of depression, in comparators without depression but with other mental health, neurodevelopmental or neurodegenerative disorders (active controls) and in healthy controls. Method Cross-sectional analysis of an opportunistic sample from England. Self-reported data were collected on demographics, diagnosis, medication, ANS symptoms (Composite Autonomic Symptom Scale-31, COMPASS-31) and fatigue (Visual Analogue Scale for Fatigue, VAS-F). A subsample completed cognitive tests (THINC-it), including the subjective Perceived Deficits Questionnaire five-item version (PDQ-5). Spearman's correlation and mediation models were used to explore the relationship between COMPASS-31, VAS-F and PDQ-5 scores. Results Data were obtained for 3345 participants, 22% with depression. The depression group had significantly (P &lt; 0.01) more severe autonomic dysregulation as measured by COMPASS-31 scores (median 30) than active (median 23) and healthy controls (median 10). The depression group had significantly higher symptom severity (P &lt; 0.01) than both control groups on the VAS-F and PDQ-5. Overall, there was a significantly positive correlation (P &lt; 0.01) between COMPASS-31, VAS-F scores (Spearman's rho rs = 0.44) and PDQ-5 scores (rs = 0.56). COMPASS-31 scores mediated greater symptom severity on the VAS-F and PDQ-5 for those with depression. COMPASS-31 scores remained significantly different between the depression group and both control groups independently of medication. Conclusions People with a diagnosis of depression report worse fatigue and cognition than active and healthy comparators; this appears to be mediated by ANS dysregulation.

Cognitive Function in People With Familial Risk of Depression

Cognitive impairment in depression is poorly understood. Family history of depression is a potentially useful risk marker for cognitive impairment, facilitating early identification and targeted intervention in those at highest risk, even if they do not themselves have depression. Several research cohorts have emerged recently that enable findings to be compared according to varying depths of family history phenotyping, in some cases also with genetic data, across the life span. To investigate associations between familial risk of depression and cognitive performance in 4 independent cohorts with varied depth of assessment, using both family history and genetic risk measures. This study used data from the Three Generations at High and Low Risk of Depression Followed Longitudinally (TGS) family study (data collected from 1982 to 2015) and 3 large population cohorts, including the Adolescent Brain Cognitive Development (ABCD) study (data collected from 2016 to 2021), National Longitudinal Study of Adolescent to Adult Health (Add Health; data collected from 1994 to 2018), and UK Biobank (data collected from 2006 to 2022). Children and adults with or without familial risk of depression were included. Cross-sectional analyses were conducted from March to June 2022. Family history (across 1 or 2 prior generations) and polygenic risk of depression. Neurocognitive tests at follow-up. Regression models were adjusted for confounders and corrected for multiple comparisons. A total of 57 308 participants were studied, including 87 from TGS (42 [48%] female; mean [SD] age, 19.7 [6.6] years), 10 258 from ABCD (4899 [48%] female; mean [SD] age, 12.0 [0.7] years), 1064 from Add Health (584 [49%] female; mean [SD] age, 37.8 [1.9] years), and 45 899 from UK Biobank (23 605 [51%] female; mean [SD] age, 64.0 [7.7] years). In the younger cohorts (TGS, ABCD, and Add Health), family history of depression was primarily associated with lower performance in the memory domain, and there were indications that this may be partly associated with educational and socioeconomic factors. In the older UK Biobank cohort, there were associations with processing speed, attention, and executive function, with little evidence of education or socioeconomic influences. These associations were evident even in participants who had never been depressed themselves. Effect sizes between familial risk of depression and neurocognitive test performance were largest in TGS; the largest standardized mean differences in primary analyses were -0.55 (95% CI, -1.49 to 0.38) in TGS, -0.09 (95% CI, -0.15 to -0.03) in ABCD, -0.16 (95% CI, -0.31 to -0.01) in Add Health, and -0.10 (95% CI, -0.13 to -0.06) in UK Biobank. Results were generally similar in the polygenic risk score analyses. In UK Biobank, several tasks showed statistically significant associations in the polygenic risk score analysis that were not evident in the family history models. In this study, whether assessed by family history or genetic data, depression in prior generations was associated with lower cognitive performance in offspring. There are opportunities to generate hypotheses about how this arises through genetic and environmental determinants, moderators of brain development and brain aging, and potentially modifiable social and lifestyle factors across the life span.

Methionine Capped Nanoparticles as Acetylcholinesterase Inhibitors

The silver and gold L-methionine capped nanoparticles (Ag and Au @LM NPs) were analyzed as prospective acetylcholinesterase (AChE) inhibitors to test their potential in the treatment of cognitive impairment in depression and Alzheimer's disease. The stability of NPs, and their ability to inhibit AChE were studied by UV-Vis and FTIR spectrophotometry. At the same time, TEM and SEM measurements, DLS, and zeta potential measurements were employed in the structural characterization of NPs. Nearly spherical, negatively charged Ag and Au @LM NPs, with 17 nm and 31 nm in diameter, respectively, showed moderate inhibitory potential toward AChE in the given frame of investigated concentrations. For both NPs IC50 is not reached. Furthermore, the adsorption of enzyme molecules on the surface of Ag and Au @LM NPs was demonstrated. Hence, our assumption is that inhibition of AChE is caused by blockage of the enzyme‘s active site due to the steric hindrance of NPs.

Predicting cognitive impairment in depression: a machine learning approach on multimodal structural neuroimaging

Predicting cognitive impairment in depression: a machine learning approach on multimodal structural neuroimaging

YY1 (Yin-Yang 1), a transcription factor regulating systemic inflammation, is involved in cognitive impairment of depression.

Clinical and preclinical studies suggest that alterations in the peripheral and brain immune system are associated with the pathophysiology of depression, also leading to changes in local glucose metabolism in the brain. Here, the authors identified Yin-Yang 1 (YY1), a transcription factor closely associated with central and peripheral inflammation. Plasma levels of YY1, interleukin (IL) 6, and IL-1β in major depressive disorder (MDD) were collected before and after treatment with vortioxetine, and correlation with clinical and cognitive scores was studied. Chronic unpredictable mild stress was treated with vortioxetine. Micropositron emission tomography (microPET) was used to analyze glucose metabolism and mRNA, and the protein level of the YY1-nuclear factor κB (NF-κB)-IL-1β inflammatory pathway were measured in related brain regions. Plasma levels of YY1 and IL-1β were significantly increased in MDD and decreased after treatment with vortioxetine. Meanwhile, the level of YY1 in plasma was negatively correlated with cognitive functions in patients with MDD and positively correlated with the level of IL-1β in plasma. Compared with the control group, in chronic unpredictable mild stress rats, (microPET)analysisshowed that the decrease of glucose metabolism in the hippocampus, entorhinal cortex, amygdala, striatum, and medial prefrontal cortex was reversed after treatment. mRNA and protein level of related molecular in YY1-NF-κB-IL-1β inflammatory pathway decreased in the hippocampus and was reversed by vortioxetine. The current study suggests that the YY1-NF-κB-IL-1β inflammatory pathway may play an essential role in both mood changes and cognitive impairment in depression, and may be associated with changes in glucose metabolism in emotion regulation and cognition. These findings provide new evidence for the inflammatory mechanisms of depression.

NANO CARRIER DRUG DELIVERY SYSTEMS FOR THE TREATMENT OF COGNITIVE DYSFUNCTION IN DEPRESSION-AN OVERVIEW ON THE NANO FORMULATIONS TARGETING TO THE BRAIN

To review and discuss the current therapeutic strategies available for the management of cognitive dysfunction in major depressive disorder with special emphasis on novel therapeutics based on nanotechnology like nano carrier delivery systems. The method entailed a review of research articles, review articles, and other internet-sourced materials. Journals, articles, and reports were thoroughly searched for the efficacy and safety of nanotechnology based newer drug delivery approaches for the management of cognitive dysfunction in major depressive disorder. The information obtained during the literature search aided in comprehending the scenario. Several new nanomedicines and nanotechnology based drug delivery systems for improving the efficacy of new and old drugs used for the management of cognitive dysfunction in major depressive disorder were reviewed. There is a dearth of sufficient studies which focus on cognitive domain in depression. Nanomedicines and nanotechnology based drug delivery systems holds tremendous potential in the management of cognitive impairment in depression as well as other neuropsychiatric disorders. It is imperative to conduct advanced studies in this regard for better therapeutic outcomes in the management of such patients.

Mechanisms of Cognitive Impairment in Depression. May Probiotics Help?

Depression is the major cause of disability globally. Apart from lowered mood and accompanying symptoms, it leads to cognitive impairment that altogether predicts disadvantaged social functioning. Reduced cognitive function in depression appears a bit neglected in the field of clinical and molecular psychiatry, while it is estimated to occur in two-thirds of depressed patients and persist in at least one third of remitted patients. This problem, therefore, requires elucidation at the biomolecular and system levels and calls for improvement in therapeutic approach. In this review study, we address the above-mentioned issues by discussing putative mechanisms of cognitive decline in depression: (1) increased oxidative stress and (2) inflammation, (3) disturbed hypothalamus-pituitary-adrenals axis, and (4) reduced monoamines functionality. Moreover, we acknowledge additional underpinnings of cognitive impairment in depressed elderly: (5) vascular-originated brain ischemia and (6) amyloid-beta plaque accumulation. Additionally, by reviewing molecular, pre-clinical and clinical evidence, we propose gut microbiota-targeted strategies as potential adjuvant therapeutics. The study provides a consolidated source of knowledge regarding mechanisms of cognitive impairment in depression and may path the way toward improved treatment options.

Constricted semantic relations in acute depression

BackgroundIt has been suggested that mood influences the breadth of associated information available for retrieval, with positive mood broadening and negative mood constricting the scope of associations. In this study, we asked whether this mood-associations connection is related to controlled processes which were linked to clinical symptoms in depression. MethodsWe used the semantic priming paradigm, which allows the dissociation of automatic and controlled processes by using short and long intervals between prime and target words. We further examined whether the strength of semantic relations (weak or strong) influence the priming effects in both neurotypical and depressed individuals. ResultsExperiment 1, testing neurotypical individuals, showed priming effects for strong semantically-related words regardless of interval length, but priming effects for weak semantically-related words were smaller in short intervals than in long intervals. Experiment 2, testing depressed individuals in long intervals, showed smaller priming effects for weak semantically-related words than shown by neurotypicals, but priming effects for strong semantically-related words which were comparable between the groups. LimitationsThis study cannot determine the source for the differences in priming effects between depressed individuals and neurotypicals, and further studies are needed. ConclusionsThis is the first study to show priming impairments in depressed individuals. We discuss our results in light of leading theories concerning cognitive impairment in depression, as well as the newly emerged field of digital psychiatry.

Be Fit, Be Sharp, Be Well: The Case for Exercise as a Treatment for Cognitive Impairment in Late-life Depression.

To lay out the argument that exercise impacts neurobiological targets common to both mood and cognitive functioning, and thus more research should be conducted on its use as an alternative or adjunctive treatment for cognitive impairment in late-life depression (LLD). This narrative review summarizes the literature on cognitive impairment in LLD, describes the structural and functional brain changes and neurochemical changes that are linked to both cognitive impairment and mood disruption, and explains how exercise targets these same neurobiological changes and can thus provide an alternative or adjunctive treatment for cognitive impairment in LLD. Cognitive impairment is common in LLD and predicts recurrence of depression, poor response to antidepressant treatment, and overall disability. Traditional depression treatment with medication, psychotherapy, or both, is not effective in fully reversing cognitive impairment for most depressed older adults. Physical exercise is an ideal treatment candidate based on evidence that it 1) is an effective treatment for depression, 2) enhances cognitive functioning in normal aging and in other patient populations, and 3) targets many of the neurobiological mechanisms that underlie mood and cognitive functioning. Results of the limited existing clinical trials of exercise for cognitive impairment in depression are mixed but overall support this contention. Although limited, existing evidence suggests exercise may be a viable alternative or adjunctive treatment to address cognitive impairment in LLD, and thus more research in this area is warranted. Moving forward, additional research is needed in large, diverse samples to translate the growing research findings into clinical practice.

Study of cognitive impairment in depression

IntroductionCognitive impairment is frequently observed in patients suffering from depression. Cognitive dysfunction play a critical role in increasing the individual’s vulnerability for the first onset, maintenance and future recurrence of depressive episodes.ObjectivesThe objectiv was to assess the cognitive impairment in patient with depressive episode.MethodsA cross sectional, hospital based study was conducted among 100 patients with depressive episodes diagnosed by International Classification of Diseases - 10 visiting outpatient and inpatient in Department of Psychiatry of Manipal Teaching Hospital, Pokhara, Nepal. The subjects were interviewed with Beck’s depression inventory, Perceived deficient questionnaire, Frontal assessment battery, Trail making test A and B and Forward and Backward Digit Span test. For the assessment of correlates, regression analyses were done using SPSS v 20.0.ResultsThe mean age of the participants was 32.47 years (SD±12.25), majority were female, married, Hindu and from urban population. Higher number of respondent were student. Most of them were educated till intermediate level and belonged to middle socioeconomic class family. Different domain of cognitive function according to severity of depression was found to be statistically significant (p&lt;0.05). This study also found that age, sex, education, medication use and Becks depression inventory score predicted the cognitive function.ConclusionsCognitive impairment is not ucommon among patient with depressive episodes. The impairment is not only seen in severe cases but also in mild to moderate cases. The assessment of cognitive deficits should be the regular part of the assessment in depressive patients.

Contemporary approaches to correction of cognitive impairment in endogenous depression

Cognitive dysfunction is one of the basic symptoms of endogenous depression, gaining much of the researchers’ interest lately. It is observed at the initial stage, at the peak intensity of depressive symptoms and even after their reduction, which leads to the persistence of residual depressive state. Cognitive impairment during the depressive episode can be detected by objective methods (clinical and neuropsychological), and their subjective importance is being revealed by standardized questionnaires. Depressed patients show lower results in executive functions, working memory, reaction speed, verbal learning, immediate and delayed recall subtests of neuropsychological batteries. There are few pharmacological agents (mostly antidepressants) with well-proven procognitive activity in depression. Besides, some new pharmacological and non-pharmacological approaches for treatment of cognitive impairment in depression have appeared lately and are described in literature as promising.