121,850 research outputs found
Family history of a mood disorder indicates a more severe bipolar disorder.
No full textBACKGROUND:
In the clinical setting, patients with bipolar disorder (BD) are often asked about potential family history (FH) of mood disorders. The aim of the present study was to examine differences between BD patients with FH of a mood disorder, and those without, on clinical, personality and social functioning characteristics, as well as on the symptomatic course of the disorder.
METHODS:
Data was collected from the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). For this report, we included 2600 patients, 1963 of those reported having a first-degree family member with a mood disorder, and 637 reported of no such FH. We investigated the impact of FH on socio-demographic, clinical, personality and quality of life variables, as well as on symptomatology during the first year of treatment.
RESULTS:
Patients reporting FH of a mood disorder had an earlier age at onset of depression/mania, more phases, rapid cycling and more suicide attempts. Across different assessments, patients with FH showed consistently elevated depressive symptoms, such as lower concentration and energy, higher suicidal ideation, as well as increased racing thoughts and distractibility within the manic spectrum of symptoms. Further, the FH group had lower quality of life, higher neuroticism and higher personality disorder scores compared to patients without FH.
LIMITATIONS:
Information on FH was obtained through the proband.
CONCLUSIONS:
Overall, BD patients reporting FH of a mood disorder showed a worse clinical profile upon presentation for treatment and a more symptomatic course of the disorder
Serotonergic genes and suicide: a systematic review.
No full textSuicide is one of the leading causes of death in the world. Its aetiology is complex and diverse, however, epidemiological studies show that suicidal behavior is partly heritable. Neurobiological evidence implicates serotonergic dysfunction in suicidality, stimulating genetic research to focus on genes related to the serotonergic system. In this paper, we review evidence from studies examining the association between various serotonergic genes (Tryptophan Hydroxylase genes: TPH1; TPH2, Serotonin Transporter gene: 5-HTTLPR in SLC6A4, Serotonin Receptor genes: HTR1A, HTR2A, HTR1B, HTR2C and Monoamine Oxidase A gene: MAOA) and suicidal behavior. The data show associations between variation on the TPH1 gene and 5-HTTLPR gene and violent suicidal behavior in Caucasian populations, with the least inconsistencies. Results are mixed for the TPH2 gene and serotonin receptor genes, but for some genes, studies that include haplotypic analyses or that examine a larger coding region of the genes tend to provide more reliable results. Findings on endophenotypes of suicidality, such as aggression and impulsivity traits, show positive associations for the TPH1, HTR2A, and MAOA genes, but need further replication, since negative associations are also occasionally reported. Since genes can only partially explain suicidal risk, several studies during the past decade have tried to incorporate environmental factors in the susceptibility model. Studies to date show that variation on the 5-HTTLPR, MAOA and HTR2A gene can interact with stressful life events to increase risk for suicidal behavior. Limitations of case-control studies are discussed and future considerations are put forward with regard to endophenotypic measurements and gene-environment interactions
Clinical, psychological and environmental predictors of prospective suicide events in patients with Bipolar Disorder.
No full textPatients with Bipolar Disorder (BD) have high rates of suicide compared to the general population. The present study investigates the predictive power of baseline clinical, psychological and environmental characteristics as risk factors of prospective suicide events (attempts and completions). Data was collected from the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study. 3083 bipolar patients were included in this report, among these 140 (4.6%) had a suicide event (8 died by suicide and 132 attempted suicide). Evaluation and assessment forms were used to collect clinical, psychological and socio-demographic information. Chi-square and independent t-tests were used to evaluate baseline characteristics. Potential prospective predictors were selected on the basis of prior literature and using a screening analysis of all risk factors that were associated with a history of suicide attempt at baseline and were tested using a Cox regression analysis. The strongest predictor of a suicide event was a history of suicide attempt (hazard ratio = 2.60, p-value < 0.001) in line with prior literature. Additional predictors were: younger age, a high total score on the personality disorder questionnaire and a high percentage of days spent depressed in the year prior to study entry. In conclusion, the present findings may help clinicians to identify patients at high risk for suicidal behavior upon presentation for treatment
Genomewide interaction and enrichment analysis on antidepressant response.
No full textBACKGROUND:
Genomewide association studies (GWASs) on antidepressant efficacy have yielded modest results. A possible reason is that response is influenced by other factors, which possibly interact with genetic variation. We used a GWAS model to predict antidepressant response, by including predictors previously known to affect response, such as quality of life (QoL). We also evaluated the association between genes, previously implicated in gene-environment (G × E) interactions, and response using an enrichment analysis.
METHOD:
We examined a sample of 1426 depressed patients from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial: 774 responders, 652 non-responders and 418,865 single nucleotide polymorphisms (SNPs) were analysed. First, in a GWAS model, we investigated whether genetic variations interact with patients' levels of QoL to predict response, after controlling for demographic characteristics, severity and population stratification. Second, we conducted an enrichment analysis exploring whether candidate genes that have emerged from prior G × E interaction studies on depression are associated with treatment response.
RESULTS:
The GWAS model, with QoL as a moderator, yielded one SNP (rs520210) associated with response in the NEDD4L gene (p = 3.64 × 10−8). In the Caucasian sample only, we observed a drop in significance for this SNP. The enrichment analysis showed that SNPs within serotonergic genes contained more significant markers that predicted response, compared with a random set of genes in the genome.
CONCLUSIONS:
Our findings point to possible target genes, which are proposed for further independent replication. Our enrichment analysis provides further support, in a genomewide context, of the role of serotonergic genes in influencing antidepressant response
The role of COMT gene variants in depression: Bridging neuropsychological, behavioral and clinical phenotypes.
No full textDepression is a common and disabling psychiatric disorder with a complex etiology, which includes predisposing risk genes and environmental stressors. Variation in the Catechol-O-Methyltransferase (COMT) gene, the Val158Met polymorphism in particular, has been extensively investigated in relation to clinical phenotypes of depression and, in parallel, neurocognitive processes. In this review, we bridge evidence from neuroimaging, behavioral and clinical studies that have examined the role of COMT variants on depression-relevant phenotypes. We observed that clinical phenotypes such as depression severity and diagnosis, or behavioral endophenotypes, are less reliably associated with COMT genetic variation. On the other hand, genetic effects are more discernible on brain systems of emotional processing. Specifically, the Met allele is associated with increased activity in limbic areas and prefrontal cortex, but is also more likely to have a better response to antidepressant treatment, compared to the Val allele. Gender and stress are important modulators of COMT genetic effects. On the basis of current evidence, we propose a tentative pathway through which the COMT gene may influence cognitive vulnerability to depression
sj-docx-1-asm-10.1177_10731911231216053 – Supplemental material for Examination of Acceptability, Feasibility, and Iatrogenic Effects of Ecological Momentary Assessment (EMA) of Suicidal Ideation
No full textSupplemental material, sj-docx-1-asm-10.1177_10731911231216053 for Examination of Acceptability, Feasibility, and Iatrogenic Effects of Ecological Momentary Assessment (EMA) of Suicidal Ideation by L. M. M. Kivelä, F. Fiß, W. van der Does and N. Antypa in Assessment</p
The 3111T/C polymorphism interacts with stressful life events to influence patterns of sleep in females.
No full textGenetic variations in clock-relevant genes have been investigated in relation to sleep abnormalities, both in healthy populations and in mood-disorder patients with inconsistent results. Environmental influences may moderate associations between genes and phenotype. The authors examined the CLOCK 3111T/C polymorphism and several variants within the PER3 gene and their possible interaction with stressful life events in a group of female volunteers (n = 415). Gene-environment (G × E) interactions and gene main effects were investigated on depressive symptoms using the Beck Depression Inventory and on change of sleep patterns (Item 16). Results showed a G × E interaction on alteration of sleeping pattern: the 3111C homozygous genotype reported greater disruption in sleep pattern after the experience of stressful life events. Within the PER3 gene, one G × E interaction was observed with rs228642 on sleep change. These findings show that the 3111T/C polymorphism is not associated with depressive symptoms, but only with symptoms of sleep change in the case of prior stressful life experiences. The combination of a sensitive genotype (3111C/C) and environmental stress increases vulnerability to circadian rhythm disruption in females
The role of serotonergic genes and environmental stress on the development of depressive symptoms and neuroticism
No full textBACKGROUND:
Depression is considered to be the result of a complicated synergy between genetic and environmental factors. Several genes of the serotonergic neurotransmission have been related to depression phenotypes, however results are inconsistent, possibly due to the oversight of the role of environmental stress.
METHODS:
We examined gene-environment (GxE) interactions with serotonergic genes on depressive symptoms and neuroticism in a homogeneous population-based sample of 415 females. We chose several genetic variants within candidate genes (SLC6A4, TPH2, HTR1A) that have been previously found to provide some evidence of association with depression outcomes.
RESULTS:
Single marker analyses showed a significant GxE interaction with several TPH2 variants, including rs4570625, on depressive symptoms. Significant GxE interactions were also observed with TPH2 haplotypes. No reliable associations were observed with SLC6A4 and HTR1A genes. We did not find any robust evidence of a direct impact of serotonergic genes on depressive symptoms or neuroticism.
LIMITATIONS:
Due to the high number of analyses conducted, results must be interpreted with caution.
CONCLUSIONS:
The present study indicates an association between TPH2 and depressive symptoms that is conditional on prior experience of stressful life events. Further evidence is provided about the role of the environment in genetic vulnerability to depressio
The 5-HTTLPR polymorphism and posttraumatic stress disorder: a meta-analysis.
No full textEnvironmental and genetic factors contribute to the development of posttraumatic stress disorder (PTSD). Variation in the 5-HTTLPR polymorphism of the serotonin transporter gene has been hypothesized to affect risk for PTSD. With the aim of investigating this association, we conducted a meta-analysis to shed light on prior controversial results and increase statistical power to detect smaller effect sizes. PubMed and ISI databases were searched for studies published until December 2012. Twelve studies have been included, all based on trauma-exposed samples. Data were analyzed with Cochrane Collaboration Review Manager Software (Version 5). Quality and publication bias were assessed. Metaregressions were performed using Comprehensive Meta-Analysis software, Version 2. Taking into account all studies, no association was found between 5-HTTLPR and PTSD (p = .10), with evidence of between-study heterogeneity, which could be partly explained by gender differences. In sensitivity analyses, we found an association between SS genotype and PTSD in high trauma-exposed participants (p < .001). To be a carrier of the SS genotype seems to represent a risk factor for PTSD in high trauma exposure. Further studies focusing on Gene × Environment interactions are needed to better understand the role of this polymorphism in PTSD
A Multi-Language Comparison of Influences on Author Verification using Character N-Grams
No full textWe create a new multi-language corpus for author verification based on Wikipedia talkpages, and evaluate the influence that differences in topic and time have on character n-gram author profiles. Topic alignment between two texts is found to increase author verification precision, and an authors writing style is found to change over time, but not more significantly after 3 years than after 1 year.Information ArchitectureWISElectrical Engineering, Mathematics and Computer Scienc
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