EEG based depression detection by machine learning: Does inner or overt speech condition provide better biomarkers when using emotion words as experimental cues?

Background: Objective diagnostic approaches need to be tested to enhance the efficacy of depression detection. Non-invasive EEG-based identification represents a promising area.

Aims: The present EEG study addresses two central questions: 1) whether inner or overt speech condition result in higher diagnositc accuracy of depression detection; and 2) does the affective nature of the presented emotion words count in such diagnostic approach.

Multicentric Assessment of a Multimorbidity-Adjusted Disability Score to Stratify Depression-Related Risks Using Temporal Disease Maps: Instrument Validation Study.

Background: Comprehensive management of multimorbidity can significantly benefit from advanced health risk assessment tools that facilitate value-based interventions, allowing for the assessment and prediction of disease progression. Our study proposes a novel methodology, the Multimorbidity-Adjusted Disability Score (MADS), which integrates disease trajectory methodologies with advanced techniques for assessing interdependencies among concurrent diseases. This approach is designed to better assess the clinical burden of clusters of interrelated diseases and enhance our ability to anticipate disease progression, thereby potentially informing targeted preventive care interventions.

Olfactory genes affect major depression in highly educated, emotionally stable, lean women: a bridge between animal models and precision medicine.

Most current approaches to establish subgroups of depressed patients for precision medicine aim to rely on biomarkers that require highly specialized assessment. Our present aim was to stratify participants of the UK Biobank cohort based on three readily measurable common independent risk factors, and to investigate depression genomics in each group to discover common and separate biological etiology. Two-step cluster analysis was run separately in males (n = 149,879) and females (n = 174,572), with neuroticism (a tendency to experience negative emotions), body fat percentage, and years spent in education as input variables.

A sound mind in a sound body: a novel concept unravelling heterogeneity of depression.

Depression is a highly prevalent and debilitating condition, yet we still lack both in-depth knowledge concerning its etiopathology and sufficiently efficacious treatment options. With approximately one third of patients resistant to currently available antidepressants there is a pressing need for a better understanding of depression, identifying subgroups within the highly heterogeneous illness category and to understand the divergent underlying biology of such subtypes, to help develop and personalise treatments. The TRAJECTOME project aims to address such challenges by (1) identifying depression-related multimorbidity subgroups and shared molecular pathways based on temporal disease profiles from healthcare systems and biobank data using machine learning approaches, and by (2) characterising these subgroups from multiple aspects including genetic variants, metabolic processes, lifestyle and environmental factors.

Genetic risk of depression is different in subgroups of dietary ratio of tryptophan to large neutral amino acids.

Manipulation of intake of serotonin precursor tryptophan has been exploited to rapidly induce and alleviate depression symptoms. While studies show that this latter effect is dependent on genetic vulnerability to depression, the effect of habitual tryptophan intake in the context of predisposing genetic factors has not been explored. Our aim was to investigate the effect of habitual tryptophan intake on mood symptoms and to determine the effect of risk variants on depression in those with high and low tryptophan intake in the whole genome and specifically in serotonin and kynurenine pathways.

A replication study separates polymorphisms behind migraine with and without depression.

The largest migraine genome-wide association study identified 38 candidate loci. In this study we assessed whether these results replicate on a gene level in our European cohort and whether effects are altered by lifetime depression. We tested SNPs of the loci and their vicinity with or without interaction with depression in regression models.

Biology of Perseverative Negative Thinking: The Role of Timing and Folate Intake.

Past-oriented rumination and future-oriented worry are two aspects of perseverative negative thinking related to the neuroticism endophenotype and associated with depression and anxiety. Our present aim was to investigate the genomic background of these two aspects of perseverative negative thinking within separate groups of individuals with suboptimal versus optimal folate intake. We conducted a genome-wide association study in the UK Biobank database ( = 72,621) on the "rumination" and "worry" items of the Eysenck Personality Inventory Neuroticism scale in these separate groups.

Increased activation of the pregenual anterior cingulate cortex to citalopram challenge in migraine: an fMRI study.

Background: The anterior cingulate cortex (ACC) is a key structure of the pain processing network. Several structural and functional alterations of this brain area have been found in migraine. In addition, altered serotonergic neurotransmission has been repeatedly implicated in the pathophysiology of migraine, although the exact mechanism is not known.

Spatiotemporal brain activation pattern following acute citalopram challenge is dose dependent and associated with neuroticism: A human phMRI study.

Background: The initial effects of selective serotonin reuptake inhibitors (SSRIs) in the human living brain are poorly understood. We carried out a 3T resting state fMRI study with pharmacological challenge to determine the brain activation changes over time following different dosages of citalopram.

Methods: During the study, 7.

The UKB envirome of depression: from interactions to synergistic effects.

Major depressive disorder is a result of the complex interplay between a large number of environmental and genetic factors but the comprehensive analysis of contributing environmental factors is still an open challenge. The primary aim of this work was to create a Bayesian dependency map of environmental factors of depression, including life stress, social and lifestyle factors, using the UK Biobank data to determine direct dependencies and to characterize mediating or interacting effects of other mental health, metabolic or pain conditions. As a complementary approach, we also investigated the non-linear, synergistic multi-factorial risk of the UKB envirome on depression using deep neural network architectures.

Significance of risk polymorphisms for depression depends on stress exposure.

Depression is a polygenic and multifactorial disorder where environmental effects exert a significant impact, yet most genetic studies do not consider the effect of stressors which may be one reason for the lack of replicable results in candidate gene studies, GWAS and between human studies and animal models. Relevance of functional polymorphisms in seven candidate genes previously implicated in animal and human studies on a depression-related phenotype given various recent stress exposure levels was assessed with Bayesian relevance analysis in 1682 subjects. This Bayesian analysis indicated a gene-environment interaction whose significance was also tested with a traditional multivariate analysis using general linear models.

Variability in the effect of 5-HTTLPR on depression in a large European population: the role of age, symptom profile, type and intensity of life stressors.

Background: Although 5-HTTLPR has been shown to influence the risk of life stress-induced depression in the majority of studies, others have produced contradictory results, possibly due to weak effects and/or sample heterogeneity.

Methods: In the present study we investigated how age, type and intensity of life-stressors modulate the effect of 5-HTTLPR on depression and anxiety in a European population cohort of over 2300 subjects. Recent negative life events (RLE), childhood adversity (CHA), lifetime depression, Brief Symptoms Inventory (BSI) depression and anxiety scores were determined in each subject.

Novel genes in Human Asthma Based on a Mouse Model of Allergic Airway Inflammation and Human Investigations.

Purpose: Based on a previous gene expression study in a mouse model of asthma, we selected 60 candidate genes and investigated their possible roles in human asthma.

Methods: In these candidate genes, 90 SNPs were genotyped using MassARRAY technology from 311 asthmatic children and 360 healthy controls of the Hungarian (Caucasian) population. Moreover, gene expression levels were measured by RT PCR in the induced sputum of 13 asthmatics and 10 control individuals.

Brain galanin system genes interact with life stresses in depression-related phenotypes.

Galanin is a stress-inducible neuropeptide and cotransmitter in serotonin and norepinephrine neurons with a possible role in stress-related disorders. Here we report that variants in genes for galanin (GAL) and its receptors (GALR1, GALR2, GALR3), despite their disparate genomic loci, conferred increased risk of depression and anxiety in people who experienced childhood adversity or recent negative life events in a European white population cohort totaling 2,361 from Manchester, United Kingdom and Budapest, Hungary. Bayesian multivariate analysis revealed a greater relevance of galanin system genes in highly stressed subjects compared with subjects with moderate or low life stress.

Bayesian systems-based genetic association analysis with effect strength estimation and omic wide interpretation: a case study in rheumatoid arthritis.

Rich dependency structures are often formed in genetic association studies between the phenotypic, clinical, and environmental descriptors. These descriptors may not be standardized, and may encompass various disease definitions and clinical endpoints which are only weakly influenced by various (e.g.

Complex analysis of multiple single nucleotide polymorphisms as putative risk factors of tooth agenesis in the Hungarian population.

Objectives: The role was studied of multiple single nucleotide polymorphisms in tooth agenesis in the Hungarian population using a complex approach.

Methods: Eight SNPs, PAX9 -912 C/T, PAX9 -1031 A/G, MSX1 3755 A/G, FGFR1 T/C rs881301, IRF6 T/C rs764093, AXIN2-8150 A/G, AXIN2-8434 A/G and AXIN2-30224 C/T, were studied in 192 hypodontia and 17 oligodontia cases and in 260 healthy volunteers. Case-control analysis was performed to test both allelic and genotypic associations as well as associations at the level of haplotypes.

Roles of genetic polymorphisms in the folate pathway in childhood acute lymphoblastic leukemia evaluated by Bayesian relevance and effect size analysis.

In this study we investigated whether polymorphisms in the folate pathway influenced the risk of childhood acute lymphoblastic leukemia (ALL) or the survival rate of the patients. For this we selected and genotyped 67 SNPs in 15 genes in the folate pathway in 543 children with ALL and 529 controls. The results were evaluated by gender adjusted logistic regression and by the Bayesian network based Bayesian multilevel analysis of relevance (BN-BMLA) methods.

Beyond structural equation modeling: model properties and effect size from a Bayesian viewpoint. An example of complex phenotype-genotype associations in depression.

Despite the rapid evolution of measurement technologies in biomedicine and genetics, most of the recent studies aiming to explore the genetic background of multifactorial diseases were only moderately successful. One of the causes of this phenomenon is that the bottleneck of genetic research is no longer the measurement process related to various laboratory technologies, but rather the analysis and interpretation of results. The commonly applied univariate methods are inadequate for exploring complex dependency patterns of multifactorial diseases which includes nearly all common diseases, such as depression, hypertension, and asthma.

Non-synonymous single nucleotide polymorphisms in genes for immunoregulatory galectins: association of galectin-8 (F19Y) occurrence with autoimmune diseases in a Caucasian population.

Background: Galectins are potent immune regulators, with galectin-8 acting as a pro-apoptotic effector on synovial fluid cells and thymocytes and stimulator on T-cells. To set a proof-of-principle example for risk assessment in autoimmunity, and for a mutation affecting physiological galectin sensor functions, a polymorphism in the coding region of the galectin-8 gene (rs2737713; F19Y) was studied for its association with two autoimmune disorders, i.e.

Evaluation of a partial genome screening of two asthma susceptibility regions using bayesian network based bayesian multilevel analysis of relevance.

Genetic studies indicate high number of potential factors related to asthma. Based on earlier linkage analyses we selected the 11q13 and 14q22 asthma susceptibility regions, for which we designed a partial genome screening study using 145 SNPs in 1201 individuals (436 asthmatic children and 765 controls). The results were evaluated with traditional frequentist methods and we applied a new statistical method, called bayesian network based bayesian multilevel analysis of relevance (BN-BMLA).

A novel galectin-1 and interleukin 2 receptor β haplotype is associated with autoimmune myasthenia gravis.

Galectin-1 (LGALS1) and interleukin receptor 2β (IL2Rβ) are regulators of T-cell activation. Here we evaluated the association of regulatory region polymorphisms of the LGALS1 (rs4820293, rs4820294) and IL2Rβ (rs743777, rs228941) genes in 146 Caucasian myasthenia gravis patients compared to 291 ethnically matched controls. A significant difference was found in the distribution of the rs4820293/rs743777 polymorphism haplotypes (p<0.

Lack of evidence for association of two functional SNPs of CHI3L1 gene (HC-gp39) with rheumatoid arthritis.

CHI3L1 gene encodes for a glycoprotein (HC-gp39 or YKL40) secreted by synovial fibroblasts, macrophages, neutrophil granulocytes and chondrocytes. Its expression is under the control of NF-kB. It is regarded as an acute phase protein, and its levels are significantly elevated in rheumatic diseases.