Stability in symptoms of anxiety and depression as a function of genotype and environment: a longitudinal twin study from ages 3 to 63 years

Nivard, Michel G.; Dolan, Conor V.; Kendler, Kenneth S.; Kan, Kees Jan; Willemsen, Gonneke; Beijsterveldt, Catharina E. M. van; Lindauer, Ramón; Beek, Jenny H. D. A. van; Geels, Lot M.; Bartels, Meike; Middeldorp, Christel M.; Boomsma, Dorret I.

doi:10.1017/s003329171400213x

Cited by 178 publications

(199 citation statements)

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“…The genetic stability in neuroticism between the ages of 14 and 31 is also similar to the genetic stability reported for symptoms of anxiety and depression, two traits strongly correlated to neuroticism (Gillespie et al, 2004b;Nivard et al, 2014). The implications of the high degree of genetic stability for genome-wide association studies (GWAS) were discussed by Wray et al (2007).…”

Section: Discussionsupporting

confidence: 54%

Genetic and Environmental Stability of Neuroticism From Adolescence to Adulthood

et al. 2015

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Longitudinal studies of neuroticism have shown that, on average, neuroticism scores decrease from adolescence to adulthood. The heritability of neuroticism is estimated between 0.30 and 0.60 and does not seem to vary greatly as a function of age. Shared environmental effects are rarely reported. Less is known about the role of genetic and environmental influences on the rank order stability of neuroticism in the period from adolescence to adulthood. We studied the stability of neuroticism in a cohort sequential (classical) twin design, from adolescence (age 14 years) to young adulthood (age 32 years). A genetic simplex model that was fitted to the longitudinal neuroticism data showed that the genetic stability of neuroticism was relatively high (genetic correlations between adjacent age bins >0.9), and increased from adolescence to adulthood. Environmental stability was appreciably lower (environmental correlations between adjacent age bins were between 0.3 and 0.6). This low stability was largely due to age-specific environmental variance, which was dominated by measurement error. This attenuated the age-to-age environmental correlations. We constructed an environmental covariance matrix corrected for this error, under the strong assumption that all age-specific environmental variance is error variance. The environmental (co)variance matrix corrected for attenuation revealed highly stable environmental influences on neuroticism (correlations between adjacent age bins were between 0.7 and 0.9). Our results indicate that both genetic and environmental influences have enduring effects on individual differences in neuroticism.

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Section: Discussionsupporting

confidence: 54%

Genetic and Environmental Stability of Neuroticism From Adolescence to Adulthood

et al. 2015

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“…Therefore, SCZ is the result of an interaction between genes and the environment [8, 9]. The importance of genetic components as well as developmental and environmental influences in SCZ has been demonstrated by family, twin, and adoption studies [10-12]. …”

Section: Introductionmentioning

confidence: 99%

Association Between Polymorphisms of the Complement 3 Gene and Schizophrenia in a Han Chinese Population

Zhang

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Schizophrenia is a severe psychiatric disorder, and complement 3 (C3) is closely related to schizophrenia. We investigated the association between C3 polymorphisms and schizophrenia in a Northeast Han Chinese population. Methods: A total of 2240 Chinese people, consisting of 1086 patients with schizophrenia and 1154 healthy controls, were recruited for this study. Ten single nucleotide polymorphisms (SNPs; rs11569562, rs344555, rs2241393, rs2241392, rs11569514, rs445750, rs451760, rs11672613, rs2230205, and rs2250656) in C3 were selected and genotyped. Results: Genotype distribution analysis indicated that rs11569514 was significantly associated with schizophrenia. In the dominant model (AA vs. GG+GA genotypes), we found a significant protective effect for rs344555 against schizophrenia (odds ratio [OR]: 0.72, 95% confidence interval [CI]: 0.53–0.99, P = 0.04). In the codominant model (TT vs. AA), we found a significant risk effect for rs11569514 on schizophrenia (OR: 4.39, 95% CI: 2.06–9.37, P < 0.001). Haplotypes, including TG (rs11569562 and rs344555), TGG (rs11569562-rs344555-rs2241393), AG (rs344555-rs2241393), CGGGT (rs11569562-rs344555-rs2241393-rs2241392-rs11569514), and ACGTG (rs11569514-rs445750-rs451760-rs11672613-rs2230205), showed either a risk or protective role for schizophrenia. Conclusions: SNP rs11569514 in C3 and haplotypes of C3 variants were associated with schizophrenia in a Han Chinese population.

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“…This confirms that depression can, to some extent, be predicted and its risk quantified, at least in adults. As for adolescents, who could be prone to exhibit more widespread and/or unstable symptoms due to greater brain plasticity during brain maturation [618,619], we observed a significant stability of anxiety-depression scores between 12 and 28 years old (Chapter 2), which has also been reported in a Dutch sample [421]. These results suggest that the comorbidity of depression cannot be completely explained by the psychodynamic theory and that there should be discrete underlying disorders that make up affective disorders and psychotic symptoms (see comorbidities from Chapter 1).…”

Section: Comorbidities Of Depressionsupporting

confidence: 78%

“…retest and internal consistency [392]. In addition, the ASR syndrome scale is heritable through adolescence [421] and captures a stable construct across age and sex [422]. DSMoriented and syndrome based scales appear to comparably predict affective disorder diagnoses [423][424][425].…”

Section: Participantsmentioning

confidence: 99%

Breaking down the genetics of depression using brain endophenotypes

Couvy‐Duchesne¹

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The Queensland Brain Institute 2 Thesis AbstractThe objective of the work presented in this thesis was to extend our understanding of depression aetiology and to identify brain MRI endophenotypes of depression. Our work builds on previous research that highlighted the genetic relationships between stress, sex and depression. In addition, MRI measurements are heritable and do not relying on selfreport. As such, they represent promising endophenotypes that could help break down further the genetics of depression.Preliminary work involved reporting depression prevalence in a young adult Australian twin sample (N=2,773) as well as comorbidity with affective and substance use disorders (Chapter 1). In addition, we demonstrated the good psychometric properties of the SPHERE questionnaire, which provides self-reported measures of anxiety-depression and chronic fatigue. Properties of the scores include: i) stochastic ordering on the sum score, ii) limited sex and age bias through adolescence, iii) high internal consistency, iv) good 3 months test-retest, v) moderate heritability, vi) significant association with lifetime MDD, social anxiety and alcohol dependence diagnoses (Chapter 2).In an older sample of Australian twins (N=5,221, Chapter 3), we performed a direct test of the diathesis-stress hypothesis in depression, which states that stressors can mediate the effect of genetic predisposition (diathesis) on the disease risk. We used Polygenic Risk Scores as a measure of diathesis and report a significant interaction with personal stressful life events, supporting the idea that stress and predisposition have a multiplicative effect on the depression liability scale. This interaction may be different between sexes as suggested by the stratified analysis.We then performed 3 analyses of resting-state fMRI from which we showed that: 1) Head motion (HM) is reliable and heritable in addition to being a major confound in fMRI analyses. However, this is unlikely to greatly confound twin studies of resting-state functional connectivity (FC). As a by-product of the analysis we showed that FC in the Broca's areas networks exhibited low to moderate test-retest and heritability (Chapter 4).2) HM is phenotypically and genetically associated with ADHD scores of Inattention and Hyperactivity/Impulsivity. This leads to most head motion image processing options to reduce power and/or to induce a sampling bias in RS-fMRI studies of ADHD. We discussed ways of circumventing this problem, via volume pruning or multivariate analysis (Chapter 5). 33) Nuisance regression (global signal regression, CompCor and HM regression) options in RS-fMRI processing have a moderate impact on the test-retest of regional homogeneity. Independently of the processing options, the low to moderate intra-class coefficients estimated in our sample may be due to insufficient scanning time (5mins 20s) and would impair our statistical power to detect RS-fMRI endophenotypes of depression (Chapter 6).Rather, we focused on structural brain images and contributed sample...

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Stability in symptoms of anxiety and depression as a function of genotype and environment: a longitudinal twin study from ages 3 to 63 years

Cited by 178 publications

References 39 publications

Genetic and Environmental Stability of Neuroticism From Adolescence to Adulthood

Genetic and Environmental Stability of Neuroticism From Adolescence to Adulthood

Association Between Polymorphisms of the Complement 3 Gene and Schizophrenia in a Han Chinese Population

Breaking down the genetics of depression using brain endophenotypes

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