Associations Between Negative Symptoms and Effort Discounting in Patients With Schizophrenia and Major Depressive Disorder.
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ABSTRACT:
SUBMITTER: Cathomas F
PROVIDER: S-EPMC8650075 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundGrowing evidence has shown that alterations in the gut microbiota composition were associated with a variety of neuropsychiatric conditions. However, whether such associations reflect causality remains unknown. We aimed to reveal the causal relationships among gut microbiota, metabolites, and neuropsychiatric disorders including Alzheimer's disease (AD), major depressive disorder (MDD), and schizophrenia (SCZ).MethodsA two-sample bi-directional Mendelian randomization analysis was performed by using genetic variants from genome-wide association studies as instrumental variables for gut microbiota, metabolites, AD, MDD, and SCZ, respectively.ResultsWe found suggestive associations of host-genetic-driven increase in Blautia (OR, 0.88; 95%CI, 0.79-0.99; P = 0.028) and elevated γ-aminobutyric acid (GABA) (0.96; 0.92-1.00; P = 0.034), a downstream product of Blautia-dependent arginine metabolism, with a lower risk of AD. Genetically increased Enterobacteriaceae family and Enterobacteriales order were potentially associated with a higher risk of SCZ (1.09; 1.00-1.18; P = 0.048), while Gammaproteobacteria class (0.90; 0.83-0.98; P = 0.011) was related to a lower risk for SCZ. Gut production of serotonin was potentially associated with an increased risk of SCZ (1.07; 1.00-1.15; P = 0.047). Furthermore, genetically increased Bacilli class was related to a higher risk of MDD (1.07; 1.02-1.12; P = 0.010). In the other direction, neuropsychiatric disorders altered gut microbiota composition.ConclusionsThese data for the first time provide evidence of potential causal links between gut microbiome and AD, MDD, and SCZ. GABA and serotonin may play an important role in gut microbiota-host crosstalk in AD and SCZ, respectively. Further investigations in understanding the underlying mechanisms of associations between gut microbiota and AD, MDD, and SCZ are required.
| S-EPMC7532639 | biostudies-literature
Project description:BackgroundMajor depressive disorder (MDD) is associated with abnormalities in financial reward processing. Previous research suggests that patients with MDD show reduced sensitivity to frequency of financial rewards. However, there is a lack of conclusive evidence from studies investigating the evaluation of financial rewards over time, an important aspect of reward processing that influences the way people plan long-term investments. Beck's cognitive model posits that patients with MDD hold a negative view of the future that may influence the amount of resources patients are willing to invest into their future selves.MethodWe administered a delay discounting task to 82 participants: 29 healthy controls, 29 unmedicated participants with fully remitted MDD (rMDD) and 24 participants with current MDD (11 on medication).ResultsPatients with current MDD, relative to remitted patients and healthy subjects, discounted large-sized future rewards at a significantly higher rate and were insensitive to changes in reward size from medium to large. There was a main effect of clinical group on discounting rates for large-sized rewards, and discounting rates for large-sized rewards correlated with severity of depressive symptoms, particularly hopelessness.ConclusionsHigher discounting of delayed rewards in MDD seems to be state dependent and may be a reflection of depressive symptoms, specifically hopelessness. Discounting distant rewards at a higher rate means that patients are more likely to choose immediate financial options. Such impairments related to long-term investment planning may be important for understanding value-based decision making in MDD, and contribute to ongoing functional impairment.
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Project description:BackgroundThere is an urgent need to identify differentiating and disease-monitoring biomarkers of schizophrenia, bipolar disorders (BD), and major depressive disorders (MDD) to improve treatment and management.MethodsWe recruited 54 first-episode schizophrenia (FES) patients, 52 BD patients, 35 MDD patients, and 54 healthy controls from inpatient and outpatient clinics. α-Melanocyte Stimulating Hormone (α-MSH), β-endorphin, neurotensin, orexin-A, oxytocin, and substance P were investigated using quantitative multiplex assay method. Psychotic symptoms were measured using the Brief Psychiatric Rating Scale (BPRS) and Positive and Negative Syndrome Scale (PANSS), manic symptoms using the Young Mania Rating Scale (YMRS), and depressive symptoms using 17 item-Hamilton Depression Rating Scale (HAMD). We additionally measured cognitive function by using a battery of tests given to all participants.Resultsα-MSH, neurotensin, orexin-A, oxytocin, and substance P were decreased in the three patient groups compared with controls. Neurotensin outperformed all biomarkers in differentiating patient groups from controls. There were no significant differences for 6 neuropeptides in their ability to differentiate between the three patient groups. Higher neurotensin was associated with better executive function across the entire sample. Lower oxytocin and higher substance p were associated with more psychotic symptoms in FES and BD groups. β-endorphin was associated with early morning wakening symptom in all three patient groups.ConclusionOur research shows decreased circulating neuropeptides have the potential to differentiate severe mental illnesses from controls. These neuropeptides are promising treatment targets for improving clinical symptoms and cognitive function in FES, BD, and MDD.
| S-EPMC10235770 | biostudies-literature
Project description:The purpose of this case-control genetic association study was to explore potential relationships between polymorphisms in the limbic system-associated membrane protein (LSAMP) gene and mood and anxiety disorders. A total of 21 single-nucleotide polymorphisms (SNPs) from the LSAMP gene were analyzed in 591 unrelated patients with the diagnoses of major depressive disorder (MDD) or panic disorder (PD) and in 384 healthy control subjects. The results showed a strong association between LSAMP SNPs and MDD, and a suggestive association between LSAMP SNPs and PD. This is the first evidence of a possible role of LSAMP gene in mood and anxiety disorders in humans.
| S-EPMC3432189 | biostudies-literature
Project description:The current prospective study investigated transactional relations between maternal depressive symptoms and children's depressive and externalizing symptoms. Participants included 240 children (M age = 11.86 years, SD = 0.56; 53.9% female) and their mothers who were part of a 6-year longitudinal study. Measures of maternal depression (Beck Depression Inventory), child depression (Children's Depression Inventory), and children's externalizing symptoms (Youth Self-Report Form) were assessed annually. Data analyses using dynamic latent difference score structural equation models indicated that the observed relations between mothers' and adolescents' symptoms were stable across the 6 years. Higher levels of maternal depressive symptoms predicted subsequent elevations in children's depressive symptoms and in their externalizing problems over time. Among mothers with high initial levels of depression, children's depressive symptoms predicted subsequent declines in mothers' depressive symptoms. Children's externalizing problems were not related to subsequent change in maternal symptoms.
| S-EPMC3402354 | biostudies-other
Project description:The lateral habenula plays a central role in reward and punishment processing and has been suggested to drive the cardinal symptom of anhedonia in depression. This hypothesis is largely based on observations of habenula hypermetabolism in animal models of depression, but the activity of habenula and its relationship with clinical symptoms in patients with depression remains unclear. High-resolution functional magnetic resonance imaging (fMRI) and computational modelling were used to investigate the activity of the habenula during a probabilistic reinforcement learning task with rewarding and punishing outcomes in 21 unmedicated patients with major depression and 17 healthy participants. High-resolution anatomical scans were also acquired to assess group differences in habenula volume. Healthy individuals displayed the expected activation in the left habenula during receipt of punishment and this pattern was confirmed in the computational analysis of prediction error processing. In depressed patients, there was a trend towards attenuated left habenula activation to punishment, while greater left habenula activation was associated with more severe depressive symptoms and anhedonia. We also identified greater habenula volume in patients with depression, which was associated with anhedonic symptoms. Habenula dysfunction may contribute to abnormal response to punishment in patients with depression, and symptoms such as anhedonia.
| S-EPMC5629818 | biostudies-literature
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:Mitochondria provide most of the energy for brain cells by the process of oxidative phosphorylation. Mitochondrial abnormalities and deficiencies in oxidative phosphorylation have been reported in individuals with schizophrenia (SZ), bipolar disorder (BD), and major depressive disorder (MDD) in transcriptomic, proteomic, and metabolomic studies. Several mutations in mitochondrial DNA (mtDNA) sequence have been reported in SZ and BD patients.Dorsolateral prefrontal cortex (DLPFC) from a cohort of 77 SZ, BD, and MDD subjects and age-matched controls (C) was studied for mtDNA sequence variations and heteroplasmy levels using Affymetrix mtDNA resequencing arrays. Heteroplasmy levels by microarray were compared to levels obtained with SNaPshot and allele specific real-time PCR. This study examined the association between brain pH and mtDNA alleles. The microarray resequencing of mtDNA was 100% concordant with conventional sequencing results for 103 mtDNA variants. The rate of synonymous base pair substitutions in the coding regions of the mtDNA genome was 22% higher (p = 0.0017) in DLPFC of individuals with SZ compared to controls. The association of brain pH and super haplogroup (U, K, UK) was significant (p = 0.004) and independent of postmortem interval time.Focusing on haplogroup and individual susceptibility factors in psychiatric disorders by considering mtDNA variants may lead to innovative treatments to improve mitochondrial health and brain function.
| S-EPMC2654519 | biostudies-literature
Project description:BackgroundThere has been mixed evidence about whether major depression predicts drinking onset. Empirical evidence about whether the heterogeneity of major depressive symptoms differentially predicts drinking onset is scarce, and potential sex- and age-variations have not been fully studied. In this study, we estimate sex- and age-specific relationships linking (a) depressed mood and/or anhedonia with drinking onset among all 'at-risk' individuals and (b) three latent depressive constructs, manifested by 13 clinical features, with drinking onset among individuals with depressed mood and/or anhedonia.MethodsStudy population was non-institutionalized civilian residents 12 years of age and older living in the United States. Major depressive symptoms and drinking onset were assessed via audio-computer-assisted self-interviews. Logistic regressions and structural equation modeling were used for analysis.ResultsAmong all 'at risk' individuals, depressed mood or anhedonia strongly predicted early-adolescent drinking onset, whereas they did not predict at-age drinking onset. Among individuals with depressed mood or anhedonia, a 3-factor model provided a good fit to the data for all sex- and age-subgroups. With the exception of early-adolescent boys, neurovegetative symptoms and suicide-related symptoms tended to positively predict underage drinking onset, whereas Low mood or energy tended to inversely predict underage drinking onset; limited evidence was found for at-age and post-21 drinking onset.LimitationsThe observational nature precludes causal inference. Few people initiated alcohol drinking later than 21 years of age, which resulted in less precise estimates.ConclusionsStrengths and directions of major depressive symptoms predicting drinking onset vary across age, sex, and depressive symptoms.
| S-EPMC7103543 | biostudies-literature
Project description:ObjectiveIn mental health care, treatment effects are commonly monitored by symptom severity measures. This study aimed to investigate the relationship between symptom severity and well-being in the treatment of patients with major depressive disorder (MDD).MethodsAdult MDD outpatients (n = 77) were administered the Quick Inventory of Depressive Symptomatology-Self-Report (QIDS-SR), the Outcome Questionnaire (OQ-45), and the Mental Health Continuum-Short Form (MHC-SF) before treatment and 6 months later.ResultsSymptom severity correlated moderately with well-being at baseline and strongly at follow-up. Reliable change index scores showed improvement on the QIDS-SR, OQ-45, and MHC-SF in 65%, 59%, and 40%, respectively. A quarter of patients improved in symptom severity but not well-being (Inventory of Depressive Symptomatology-Self-Report [IDS-SR]: 25%; OQ-45: 24%).ConclusionFindings suggest that symptom severity and subjective well-being are related, but distinct concepts. Several reasons for the stronger improvements in symptoms than in well-being are discussed.
| S-EPMC8246916 | biostudies-literature