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1.
Sci Rep ; 10(1): 22394, 2020 12 28.
Artigo em Inglês | MEDLINE | ID: mdl-33372187

RESUMO

A complex interplay between genetic and environmental factors determines the individual risk of depressive disorders. Vitamin D has been shown to stimulate the expression of the tryptophan hydroxylase 2 (TPH2) gene, which is the rate-limiting enzyme for serotonin production in the brain. Therefore, we investigate the hypothesis that serum vitamin D levels moderate the interaction between the serotonin transporter promotor gene polymorphism (5-HTTLPR) and childhood abuse in depressive disorders. Two independent samples from the Study of Health in Pomerania (SHIP-LEGEND: n = 1 997; SHIP-TREND-0: n = 2 939) were used. Depressive disorders were assessed using questionnaires (BDI-II, PHQ-9) and interview procedures (DSM-IV). Besides serum vitamin D levels (25(OH)D), a functional polymorphism (rs4588) of the vitamin D-binding protein is used as a proxy for 25(OH)D. S-allele carriers with childhood abuse and low 25(OH)D levels have a higher mean BDI-II score (13.25) than those with a higher 25(OH)D level (9.56), which was not observed in abused LL-carriers. This significant three-way interaction was replicated in individuals with lifetime major depressive disorders when using the rs4588 instead of 25(OH)D (p = 0.0076 in the combined sample). We conclude that vitamin D relevantly moderates the interaction between childhood abuse and the serotonergic system, thereby impacting vulnerability to depressive disorders.

2.
Hum Brain Mapp ; 2020 Jun 29.
Artigo em Inglês | MEDLINE | ID: mdl-32596977

RESUMO

The ENIGMA group on Generalized Anxiety Disorder (ENIGMA-Anxiety/GAD) is part of a broader effort to investigate anxiety disorders using imaging and genetic data across multiple sites worldwide. The group is actively conducting a mega-analysis of a large number of brain structural scans. In this process, the group was confronted with many methodological challenges related to study planning and implementation, between-country transfer of subject-level data, quality control of a considerable amount of imaging data, and choices related to statistical methods and efficient use of resources. This report summarizes the background information and rationale for the various methodological decisions, as well as the approach taken to implement them. The goal is to document the approach and help guide other research groups working with large brain imaging data sets as they develop their own analytic pipelines for mega-analyses.

3.
Mol Genet Genomic Med ; 8(9): e1345, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32558353

RESUMO

BACKGROUND: The mineralocorticoid receptor (MR) in the brain has a key role in the regulation of the central stress response and is associated with memory performance. We investigated whether the genetic polymorphisms rs5522 and rs2070951 of NR3C2 showed main and interactive effects with childhood trauma on memory decline. METHODS: Declarative memory was longitudinally assessed in 1,318 participants from the community-dwelling Study of Health in Pomerania using the Verbal Learning and Memory Test (VLMT). In a subsample of 377 participants aged 60 and older, the Mini-Mental Status Examination (MMSE) was additionally applied. Mean follow-up time for the VLMT and MMSE were 6.4 and 10.7 years, respectively. RESULTS: Homozygous carriers of the G allele of rs2070951 (p < .01) and of the A allele of rs5522 (p < .001) showed higher immediate recall of words as compared to carriers of C allele (rs2070951) or the G allele (rs5522). The CG haplotype was associated with decreased recall (p < .001). Likewise, in the subsample of older patients, the AA genotype of rs5522 was associated with higher MMSE scores (p < .05). CG haplotypes showed significantly reduced MMSE scores in comparison to the reference haplotype (ß = -0.60; p < .01). CONCLUSIONS: Our results indicate that the GG genotype of rs2070951 as well as the AA genotype of rs5522 are associated with diminished memory decline.

5.
Mol Psychiatry ; 2020 May 28.
Artigo em Inglês | MEDLINE | ID: mdl-32467648

RESUMO

Emerging evidence suggests that obesity impacts brain physiology at multiple levels. Here we aimed to clarify the relationship between obesity and brain structure using structural MRI (n = 6420) and genetic data (n = 3907) from the ENIGMA Major Depressive Disorder (MDD) working group. Obesity (BMI > 30) was significantly associated with cortical and subcortical abnormalities in both mass-univariate and multivariate pattern recognition analyses independent of MDD diagnosis. The most pronounced effects were found for associations between obesity and lower temporo-frontal cortical thickness (maximum Cohen´s d (left fusiform gyrus) = -0.33). The observed regional distribution and effect size of cortical thickness reductions in obesity revealed considerable similarities with corresponding patterns of lower cortical thickness in previously published studies of neuropsychiatric disorders. A higher polygenic risk score for obesity significantly correlated with lower occipital surface area. In addition, a significant age-by-obesity interaction on cortical thickness emerged driven by lower thickness in older participants. Our findings suggest a neurobiological interaction between obesity and brain structure under physiological and pathological brain conditions.

6.
Nat Genet ; 52(4): 437-447, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32231276

RESUMO

Minimal phenotyping refers to the reliance on the use of a small number of self-reported items for disease case identification, increasingly used in genome-wide association studies (GWAS). Here we report differences in genetic architecture between depression defined by minimal phenotyping and strictly defined major depressive disorder (MDD): the former has a lower genotype-derived heritability that cannot be explained by inclusion of milder cases and a higher proportion of the genome contributing to this shared genetic liability with other conditions than for strictly defined MDD. GWAS based on minimal phenotyping definitions preferentially identifies loci that are not specific to MDD, and, although it generates highly predictive polygenic risk scores, the predictive power can be explained entirely by large sample sizes rather than by specificity for MDD. Our results show that reliance on results from minimal phenotyping may bias views of the genetic architecture of MDD and impede the ability to identify pathways specific to MDD.


Assuntos
Transtorno Depressivo Maior/genética , Predisposição Genética para Doença/genética , Adulto , Idoso , Transtorno Bipolar/genética , Feminino , Estudo de Associação Genômica Ampla/métodos , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Herança Multifatorial/genética , Fenótipo , Polimorfismo de Nucleotídeo Único/genética , Fatores de Risco , Sensibilidade e Especificidade
7.
Mol Psychiatry ; 25(7): 1430-1446, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-31969693

RESUMO

Depression is more frequent among individuals exposed to traumatic events. Both trauma exposure and depression are heritable. However, the relationship between these traits, including the role of genetic risk factors, is complex and poorly understood. When modelling trauma exposure as an environmental influence on depression, both gene-environment correlations and gene-environment interactions have been observed. The UK Biobank concurrently assessed Major Depressive Disorder (MDD) and self-reported lifetime exposure to traumatic events in 126,522 genotyped individuals of European ancestry. We contrasted genetic influences on MDD stratified by reported trauma exposure (final sample size range: 24,094-92,957). The SNP-based heritability of MDD with reported trauma exposure (24%) was greater than MDD without reported trauma exposure (12%). Simulations showed that this is not confounded by the strong, positive genetic correlation observed between MDD and reported trauma exposure. We also observed that the genetic correlation between MDD and waist circumference was only significant in individuals reporting trauma exposure (rg = 0.24, p = 1.8 × 10-7 versus rg = -0.05, p = 0.39 in individuals not reporting trauma exposure, difference p = 2.3 × 10-4). Our results suggest that the genetic contribution to MDD is greater when reported trauma is present, and that a complex relationship exists between reported trauma exposure, body composition, and MDD.

8.
Artigo em Inglês | MEDLINE | ID: mdl-31518608

RESUMO

OBJECTIVE: Low levels of vitamin D were found to be associated with different mental disorders. However, the role of vitamin D in the pathogenesis of PTSD is unclear. In this study, we aimed at investigating whether PTSD is linked to reduced vitamin D levels and vitamin D deficiency. Moreover, we sought to investigate the role of the vitamin D-binding protein (also group-specific component or Gc) by testing if two functional polymorphisms (rs4588 and rs7041) were associated with vitamin D levels and PTSD. METHODS: Serum levels of total 25(OH)D were measured in a general-population sample of the Study of Health in Pomerania (SHIP-1). The number of traumatic events and status of PTSD were assessed using the PTSD module of the Structured Clinical Interview for the DSM-IV. Study participants were genotyped for rs4588 and rs7041. Associations of 25(OH)D levels and the genotypes with PTSD were tested in subjects with at least one traumatic event (n = 1653). RESULTS: 25(OH)D levels were inversely (OR: 0.96; p = 0.044) and vitamin D deficiency was positively (OR = 2.02; p = 0.028) associated with PTSD. Both polymorphisms of the Gc were associated with 25(OH)D levels and PTSD: Carriers of the CC-genotype of rs4588 showed significantly higher 25(OH)D levels (ß = 0.179, p < 0.001) and lower odds for PTSD (OR = 0.35; p = 0.023) compared to the AA-genotype. Likewise, carriers of the TT-allele of rs7041 showed lower 25(OH)D levels (-0.122; p < 0.001) and increased odds for PTSD (OR = 2.80; p = 0.015) compared to the GG-genotype. CONCLUSIONS: Our results suggest that an altered vitamin D metabolism may be involved in the pathophysiology of PTSD. Also, genotypes of the Gc and thus Gc serum levels may impact on PTSD development over and above the effects of 25(OH)D. Our findings contribute to explain the associations of PTSD with different mental and physical disorders.

9.
Biol Psychiatry ; 87(5): 419-430, 2020 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-31570195

RESUMO

BACKGROUND: The prevalence of depression is higher in individuals with autoimmune diseases, but the mechanisms underlying the observed comorbidities are unknown. Shared genetic etiology is a plausible explanation for the overlap, and in this study we tested whether genetic variation in the major histocompatibility complex (MHC), which is associated with risk for autoimmune diseases, is also associated with risk for depression. METHODS: We fine-mapped the classical MHC (chr6: 29.6-33.1 Mb), imputing 216 human leukocyte antigen (HLA) alleles and 4 complement component 4 (C4) haplotypes in studies from the Psychiatric Genomics Consortium Major Depressive Disorder Working Group and the UK Biobank. The total sample size was 45,149 depression cases and 86,698 controls. We tested for association between depression status and imputed MHC variants, applying both a region-wide significance threshold (3.9 × 10-6) and a candidate threshold (1.6 × 10-4). RESULTS: No HLA alleles or C4 haplotypes were associated with depression at the region-wide threshold. HLA-B*08:01 was associated with modest protection for depression at the candidate threshold for testing in HLA genes in the meta-analysis (odds ratio = 0.98, 95% confidence interval = 0.97-0.99). CONCLUSIONS: We found no evidence that an increased risk for depression was conferred by HLA alleles, which play a major role in the genetic susceptibility to autoimmune diseases, or C4 haplotypes, which are strongly associated with schizophrenia. These results suggest that any HLA or C4 variants associated with depression either are rare or have very modest effect sizes.

10.
Child Abuse Negl ; 101: 104311, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31877447

RESUMO

BACKGROUND: Previous studies suggested that childhood maltreatment is associated with altered memory performance in adulthood. Deficits in identifying and describing feelings as captured by the alexithymia construct are strongly linked with childhood trauma and may mediate the associations with memory function. OBJECTIVE: To investigate the associations of childhood trauma with verbal declarative memory performance and the putative mediating role of alexithymia. METHOD: Associations of the different dimensions of childhood trauma with adult declarative memory performance were tested in two large, independent general population samples comprising a total of N = 5574 participants. Moreover, we tested whether associations were mediated by alexithymia. RESULTS: In both samples, childhood emotional neglect, but not abuse emerged as a negative statistical predictor of early (sample 1: ß=-1.79; p < 0.001, sample 2: ß=-0.26; p < 0.001) as well as delayed recall (ß=-0.78; p < 0.001; ß=-0.24; p < 0.05). Likewise, childhood emotional neglect was the strongest predictor for alexithymia (ß = 3.2; p < 0.001; ß = 3.54; p < 0.001). Finally, the association between childhood emotional neglect and early (Total Mediated Effect (TME): 13.2, CI: 0.087-0.302; TME: 20.1; CI: 0.123-0.619) as well as late recall (TME: 13.2, CI: 0.086-0.301; TME: 9; CI: -0.442-0.699) was significantly mediated by alexithymia. CONCLUSIONS: Our findings suggest that childhood emotional neglect is particularly detrimental to memory functioning in adulthood. In comparison, childhood abuse was not associated with reduced declarative memory capacity. Our results contribute to explain the mechanism underlying the relation of childhood trauma and memory deficits: Finding specific associations with emotional neglect and a mediating role of alexithymia highlights the relevance of emotion processing capacities for memory functioning.

11.
Neuropsychopharmacology ; 44(12): 2030-2037, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31284290

RESUMO

Childhood traumatization (CT) is associated with the development of several neuropsychiatric disorders in later life. Experimental data in animals and observational data in humans revealed evidence for biological alterations in response to CT that may contribute to its long-term consequences. This includes epigenetic changes in miRNA levels that contribute to complex alterations of gene expression. We investigated the association between CT and 121 miRNAs in a target sample of N = 150 subjects from the general population and patients from the Department of Psychiatry. We hypothesized that CT exhibits a long-term effect on miRNA plasma levels. We supported our findings using bioinformatics tools and databases. Among the 121 miRNAs 22 were nominally significantly associated with CT and four of them (let-7g-5p, miR-103a-3p, miR-107, and miR-142-3p) also after correction for multiple testing; most of them were previously associated with Alzheimer's disease (AD) or depression. Pathway analyses of target genes identified significant pathways involved in neurodevelopment, inflammation and intracellular transduction signaling. In an independent general population sample (N = 587) three of the four miRNAs were replicated. Extended analyses in the general population sample only (N = 687) showed associations of the four miRNAs with gender, memory, and brain volumes. We gained increasing evidence for a link between CT, depression and AD through miRNA alterations. We hypothesize that depression and AD not only share environmental factors like CT but also biological factors like altered miRNA levels. This miRNA pattern could serve as mediating factor on the biological path from CT to adult neuropsychiatric disorders.


Assuntos
Experiências Adversas da Infância , MicroRNAs/sangue , Adulto , Epigênese Genética , Feminino , Substância Cinzenta/patologia , Hipocampo/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem
12.
Psychoneuroendocrinology ; 107: 232-240, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31174161

RESUMO

OBJECTIVE: Previous evidence suggested lasting and cumulative effects of traumatization on the renin-angiotensin-aldosterone-system (RAAS). However, it is unclear whether traumas during childhood and those experienced in adulthood differentially impact the RAAS. In this study, we sought to investigate main and putative interactive effects of childhood and adulthood trauma on RAAS functioning. METHODS: Plasma concentrations of renin and aldosterone were measured in a general population sample (n = 2016). Childhood trauma was assessed using the Childhood Trauma Questionnaire (CTQ), adulthood trauma was measured using the PTSD module of the Structured Clinical Interview of the DSM-IV. Linear regression models were calculated to assess the relations between childhood or adulthood traumatization with renin and aldosterone concentrations. RESULTS: Exposure to (ß = 0.094; p = 0.01), severity of childhood trauma (ß = 0.004; p = 0.01) were associated with increased aldosterone, but not renin levels. Results were carried by all dimensions of abuse, while childhood neglect was not associated with altered RAAS activity. In contrast, adulthood traumas (ß = 0.113; p < 0.01) were significantly associated with increased renin concentrations. Subjects with PTSD (renin: ß = 0.345; p = 0.01; aldosterone: ß = 0.232; p = 0.04) and those who had been exposed to both childhood and adulthood trauma showed increases in renin (ß = 0.180; p < 0.01) and aldosterone (ß = 0.340; p < 0.01) levels. DISCUSSION: These findings indicate that trauma is associated with differential alterations of the RAAS depending on the time of traumatization. Moreover, exposure to childhood or adulthood trauma may act synergistically on the RAAS, resulting in severe dysregulation of the RAAS. The results contribute to explain associations between trauma and enhanced risk for physical disease.


Assuntos
Fatores Etários , Sistema Renina-Angiotensina/fisiologia , Ferimentos e Lesões/metabolismo , Adulto , Experiências Adversas da Infância , Idoso , Aldosterona/sangue , Angiotensinas , Pressão Sanguínea , Feminino , Alemanha , Humanos , Masculino , Pessoa de Meia-Idade , Renina/sangue , Transtornos de Estresse Pós-Traumáticos/metabolismo , Transtornos de Estresse Pós-Traumáticos/fisiopatologia , Estresse Psicológico , Ferimentos e Lesões/fisiopatologia
15.
Neuropsychopharmacology ; 44(5): 930-938, 2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30700816

RESUMO

DNA methylation of the FKBP5 gene is assumed to alter FKBP5 expression and hence the synthesis of the FK506 binding protein 51, a central element of a genomic negative feedback loop for glucocorticoid receptor signaling. The present study aimed to replicate and extend previously reported influences of FKBP5 genotypes, childhood maltreatment and depression on methylation levels of five CpG sites in intron 7 of the FKBP5 gene in a large population-based sample. Besides the single nucleotide polymorphism (SNP) rs1360780, associations of the FKBP5 methylation with 22 other, unlinked FKBP5 SNPs as well as associations between FKBP5 methylation levels and transcription levels were investigated. Using whole-blood methylation of 3965 subjects of the Study of Health in Pomerania (SHIP) reduced methylation levels in TT allele carriers of rs1360780 (OR = 0.975, p = .005) and currently depressed subjects (OR = 0.995, p = 0.005) were found. Further, an impact of two yet undescribed SNPs (rs6910300, rs7771727) on methylation levels was observed. However, main and interactive effects for childhood maltreatment and lifetime major depressive disorder observed in previous studies could not be replicated. Finally, FKBP5 methylation levels were not related to FKBP5 transcription levels in whole blood. Thus, the present study verified the associations of FKBP5 genotypes and state depression on the FKBP5 methylation levels of five CpG sites in intron 7. However, FKBP5 methylation of these five CpG sites could not be validated as a valuable clinical biomarker for biological long-term effects of childhood maltreatment or lifetime depression.


Assuntos
Sobreviventes Adultos de Maus-Tratos Infantis , Experiências Adversas da Infância , Transtorno Depressivo/etiologia , Transtorno Depressivo/genética , Sistema de Registros , Proteínas de Ligação a Tacrolimo/genética , Adulto , Sobreviventes Adultos de Maus-Tratos Infantis/estatística & dados numéricos , Experiências Adversas da Infância/estatística & dados numéricos , Idoso , Metilação de DNA/genética , Transtorno Depressivo/epidemiologia , Feminino , Seguimentos , Alemanha/epidemiologia , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem
16.
Psychiatry Res ; 271: 405-411, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30530059

RESUMO

Previous evidence showed associations of alexithymia with altered declarative memory performance. However, these findings were not fully consistent and the underlying mechanism remains unclear. Alexithymic subjects may be at specific risk for chronic psychosocial stress, which in turn represents a predictor for poorer memory performance. We investigated independent and interaction effects of alexithymia and chronic perceived stress on declarative memory performance. Data were used from two independent general-population samples from the Study of Health in Pomerania (SHIP). In sample 1 (N = 1981), the Auditory Verbal Learning Test, the Toronto Alexithymia Scale (TAS-20) and the Screening Scale for Chronic Stress (SSCS) were applied. In sample 2 (N = 3799), the word list of the Nuremburg Age Inventory and TAS-20 were administered to replicate findings. Alexithymia was significantly associated with poorer immediate and delayed word recall. Chronic stress negatively predicted immediate, but not delayed recall. Alexithymia and particularly "Difficulties Identifying Feelings" showed significant associations with chronic perceived stress. Our findings provide clear evidence for an association of alexithymia with impaired declarative memory performance for words. The strong association of alexithymia with perceived chronic stress could contribute to explain the association of alexithymia with stress-related disorders.


Assuntos
Sintomas Afetivos/fisiopatologia , Transtornos da Memória/fisiopatologia , Rememoração Mental/fisiologia , Estresse Psicológico/fisiopatologia , Adulto , Sintomas Afetivos/epidemiologia , Idoso , Comorbidade , Estudos Transversais , Feminino , Alemanha/epidemiologia , Humanos , Masculino , Transtornos da Memória/epidemiologia , Pessoa de Meia-Idade , Estresse Psicológico/epidemiologia
17.
J Psychosom Res ; 115: 14-23, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30470312

RESUMO

OBJECTIVE: Alexithymia, neuroticism, and extraversion have been described as relevant predictors of mental and physical health conditions, but their putative interactive effects remain poorly understood and their prospective effects are not well studied. The present study has investigated the differential contributions of distinct personality traits in predicting mental and somatic health symptoms in cross-sectional and longitudinal analyses. METHODS: Additive and interactive effects of neuroticism and extraversion (NEO-FFI), the TAS-20 total score (20-Item Toronto Alexithymia Scale) and its factors (Difficulty Identifying Feelings (DIF), Difficulty Describing Feelings (DDF) and External Oriented Thinking (EOT)) have been investigated on depressive symptoms, the number of chronic diseases, somatic and mental subjective health complaints. Analyses have been based on data from the population-based "Study of Health in Pomerania" (SHIP) in cross-sectional (N = 1704) and longitudinal (N = 1244) analyses. RESULTS: In cross-sectional and longitudinal analyses, additive associations of the TAS-20 total score and neuroticism on somatic and mental health complaints have been observed. The effects of the TAS-20 total score have been mainly carried by DIF. Further, in interaction effetcs extraversion has attenuated the negative impact of neuroticism, whereas DIF has augmented it. CONCLUSION: The present study is the first demonstrating longitudinal effects of alexithymia, particularly DIF, neuroticism, and extraversion in predicting mental and somatic health symptoms. Associations between DIF, neuroticism, and extraversion have been additive and interactive. Hence, subjects high in neuroticism and DIF but low in extraversion have reported most health symptoms and thus might be in need for prevention strategies. Treatments chould be adapted to the associated combination of the personality characteristics.


Assuntos
Emoções/fisiologia , Extroversão Psicológica , Saúde Mental/tendências , Neuroticismo/fisiologia , Estudos Transversais , Feminino , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos
18.
BMC Psychiatry ; 18(1): 105, 2018 04 18.
Artigo em Inglês | MEDLINE | ID: mdl-29669535

RESUMO

BACKGROUND: Life events (LEs) are associated with future physical and mental health. They are crucial for understanding the pathways to mental disorders as well as the interactions with biological parameters. However, deeper insight is needed into the complex interplay between the type of LE, its subjective evaluation and accompanying factors such as social support. The "Stralsund Life Event List" (SEL) was developed to facilitate this research. METHODS: The SEL is a standardized interview that assesses the time of occurrence and frequency of 81 LEs, their subjective emotional valence, the perceived social support during the LE experience and the impact of past LEs on present life. Data from 2265 subjects from the general population-based cohort study "Study of Health in Pomerania" (SHIP) were analysed. Based on the mean emotional valence ratings of the whole sample, LEs were categorized as "positive" or "negative". For verification, the SEL was related to lifetime major depressive disorder (MDD; Munich Composite International Diagnostic Interview), childhood trauma (Childhood Trauma Questionnaire), resilience (Resilience Scale) and subjective health (SF-12 Health Survey). RESULTS: The report of lifetime MDD was associated with more negative emotional valence ratings of negative LEs (OR = 2.96, p < 0.0001). Negative LEs (b = 0.071, p < 0.0001, ß = 0.25) and more negative emotional valence ratings of positive LEs (b = 3.74, p < 0.0001, ß = 0.11) were positively associated with childhood trauma. In contrast, more positive emotional valence ratings of positive LEs were associated with higher resilience (b = - 7.05, p < 0.0001, ß = 0.13), and a lower present impact of past negative LEs was associated with better subjective health (b = 2.79, p = 0.001, ß = 0.05). The internal consistency of the generated scores varied considerably, but the mean value was acceptable (averaged Cronbach's alpha > 0.75). CONCLUSIONS: The SEL is a valid instrument that enables the analysis of the number and frequency of LEs, their emotional valence, perceived social support and current impact on life on a global score and on an individual item level. Thus, we can recommend its use in research settings that require the assessment and analysis of the relationship between the occurrence and subjective evaluation of LEs as well as the complex balance between distressing and stabilizing life experiences.


Assuntos
Acontecimentos que Mudam a Vida , Saúde Mental , Resiliência Psicológica , Inquéritos e Questionários/normas , Adulto , Estudos de Coortes , Transtorno Depressivo Maior/psicologia , Emoções , Feminino , Alemanha , Humanos , Masculino , Pessoa de Meia-Idade , Psicometria , Adulto Jovem
20.
Am J Med Genet B Neuropsychiatr Genet ; 177(1): 40-49, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-29159863

RESUMO

Gene by environment (GxE) interaction studies have investigated the influence of a number of candidate genes and variants for major depressive disorder (MDD) on the association between childhood trauma and MDD. Most of these studies are hypothesis driven and investigate only a limited number of SNPs in relevant pathways using differing methodological approaches. Here (1) we identified 27 genes and 268 SNPs previously associated with MDD or with GxE interaction in MDD and (2) analyzed their impact on GxE in MDD using a common approach in 3944 subjects of European ancestry from the Psychiatric Genomics Consortium who had completed the Childhood Trauma Questionnaire. (3) We subsequently used the genome-wide SNP data for a genome-wide case-control GxE model and GxE case-only analyses testing for an enrichment of associated SNPs. No genome-wide significant hits and no consistency among the signals of the different analytic approaches could be observed. This is the largest study for systematic GxE interaction analysis in MDD in subjects of European ancestry to date. Most of the known candidate genes/variants could not be supported. Thus, their impact on GxE interaction in MDD may be questionable. Our results underscore the need for larger samples, more extensive assessment of environmental exposures, and greater efforts to investigate new methodological approaches in GxE models for MDD.


Assuntos
Depressão/genética , Transtorno Depressivo Maior/genética , Estudos de Casos e Controles , Depressão/etiologia , Transtorno Depressivo Maior/etiologia , Grupo com Ancestrais do Continente Europeu/genética , Feminino , Interação Gene-Ambiente , Predisposição Genética para Doença , Estudo de Associação Genômica Ampla/métodos , Humanos , Acontecimentos que Mudam a Vida , Masculino , Polimorfismo de Nucleotídeo Único/genética , Fatores de Risco
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