Mediation of the influence of childhood maltreatment on depression relapse by cortical structure: a 2-year longitudinal observational study

Opel, Nils; Redlich, Ronny; Dohm, Katharina; Zaremba, Dario; Goltermann, Janik; Repple, Jonathan; Kaehler, Claas; Grotegerd, Dominik; Leehr, Elisabeth J.; Böhnlein, Joscha; Förster, Katharina; Meinert, Susanne; Enneking, Verena; Sindermann, Lisa; Dzvonyar, Fanni; Emden, Daniel; Leenings, Ramona; Winter, Nils R.; Hahn, Tim; Kugel, Harald; Heindel, Walter; Buhlmann, Ulrike; Baune, Bernhard T.; Arolt, Volker; Dannlowski, Udo

doi:10.1016/s2215-0366(19)30044-6

Cited by 115 publications

(84 citation statements)

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“…Epidemiological studies encouraged that ELS could possibly increase the risk of depression and enhance the adverse effect of later life stress. However, different types of early adversities and sex had considerable effects on the consequences (Kim et al, 2013;Culpin et al, 2015;St Clair et al, 2015;Bjorkenstam et al, 2017;Dahl et al, 2017;Frodl et al, 2017;Opel et al, 2019). The epigenetic alterations may help to explain how ELS modulated the epigenetic reprogramming and what the effect of these alterations was.…”

Section: Conclusion and Discussionmentioning

confidence: 99%

“…The HPA axis plays a critical role in the response to stress, and a disturbance of the HPA axis results in vulnerability for depression (Bjorkenstam et al, 2017;Reus et al, 2017). It is well-documented that ELS enhanced the vulnerability for depression (Kim et al, 2013;Culpin et al, 2015;St Clair et al, 2015;Airagnes et al, 2016;Williams et al, 2016;Bjorkenstam et al, 2017;Dahl et al, 2017;Opel et al, 2019;Tracy et al, 2019). Depressed subjects may bear the increased level of plasma cortisol of excessive stressinduced and impaired functions of the glucocorticoid receptors (GR) (Malhi and Mann, 2018).…”

Section: Definition Of Depressionmentioning

confidence: 99%

“…On the other hand, ELS caused epigenetic changes in the HPA axis, serotonin, dopamine, and some neuropeptides (McGowan et al, 2009;Roth et al, 2009;Bai et al, 2012;Kang et al, 2013;Ouellet-Morin et al, 2013;Zhang et al, 2015;Bahi, 2016;Bustamante et al, 2016;Tyrka et al, 2016;Williams et al, 2016;Wang et al, 2017). Therefore, epigenetic events bridge the connection between ELS and depression and some studies have proven the effect of epigenetic changes on the accumulating risk of developing depression in those who were subjected to ELS (Kang et al, 2013;Melas et al, 2013;Wankerl et al, 2014;Cecil et al, 2016;Tyrka et al, 2016;Dickson et al, 2018;Opel et al, 2019). However, though being exposed to ELS increased depressive incidents, not all individuals who suffered ELS acquired depression.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Early Life Stress on the Epigenetic Profiles in Depression

Xie

et al. 2020

Front. Cell Dev. Biol.

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Depression is one of the most common mental disorders and has caused an overwhelming burden on world health. Abundant studies have suggested that early life stress may grant depressive-like phenotypes in adults. Childhood adversities that occurred in the developmental period amplified stress events in adulthood. Epigenetic-environment interaction helps to explain the role of early life stress on adulthood depression. Early life stress shaped the epigenetic profiles of the HPA axis, monoamine, and neuropeptides. In the context of early adversities increasing the risk of depression, early life stress decreased the activity of the glucocorticoid receptors, halted the circulation and production of serotonin, and reduced the molecules involved in modulating the neurogenesis and neuroplasticity. Generally, DNA methylation, histone modifications, and the regulation of non-coding RNAs programmed the epigenetic profiles to react to early life stress. However, genetic precondition, subtypes of early life stress, the timing of epigenetic status evaluated, demographic characteristics in humans, and strain traits in animals favored epigenetic outcomes. More research is needed to investigate the direct evidence for how early life stress-induced epigenetic changes contribute to the vulnerability of depression.

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Section: Conclusion and Discussionmentioning

confidence: 99%

Section: Definition Of Depressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of Early Life Stress on the Epigenetic Profiles in Depression

Xie

et al. 2020

Front. Cell Dev. Biol.

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“…Prospective studies indicate that children and adolescents exposed to emotional, neglect and other forms of maltreatment are more likely to develop depression [30,31]. In these studies childhood maltreatment was specifically associated with depression relapse and reduced cortical surface brain area [32].…”

Section: Introductionmentioning

confidence: 89%

Self-esteem and other risk factors for depressive symptoms among adolescents in United Arab Emirates

et al. 2020

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Background Little is known about depressive symptoms among adolescents in the United Arab Emirates (UAE). This study aimed to identify the prevalence of depression and its association with selfesteem, individual, parental and family factors among adolescents aged 12 to 18 in UAE. Methods Six hundred adolescents, aged 12 to 18 years were recruited from 4 of 111 schools in a cross-sectional study. We administered Beck Depression Inventory Scale and Rosenberg Self-esteem Scale to measure self-report symptoms of depression and self-esteem. We used multiple linear regression to identify significant predictors of depression. Results Over 86% of the identified sample participated to the survey. The mean age of the sample was 14.3 (±1.3) with an excess of girls (61%). Depressive symptoms were detected in 17.2% (95% CI 14.2-20.7). There was an inverse relationship between self-esteem scores and depressive symptoms. Positive predictors of depressive symptoms, having controlled for age, gender, and ethnicity included experiencing neglect, being verbally abused in school, having no monthly allowance to spend in school, a history of physical morbidities requiring treatment, being a current or past smoker and a low family income. Conclusion The high prevalence of depressive symptoms measured in this survey suggests a significant public health problem among adolescents in the UAE. Public health interventions aimed at

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“…Nonetheless, a recent longitudinal study showed that lower surface area was specifically observed in young people experiencing depressive symptoms in early adolescence but not in those developing depressive symptoms later in adolescence, and that lower surface area was already observable in young people with subclinical depressive symptoms, not all of whom will develop a fullthreshold MDD diagnosis 36 . Thus, cortical surface area reductions may represent an early developing subtype of depressive disorder, shaped by genetic factors or early life adversity (prenatal 73,74 or perinatal or during childhood [75][76][77], and potentially precede the onset of MDD. This hypothesis is consistent with the observation that, compared with cortical thickness, cortical surface area has a higher genetic heritability 27,64,78 , has a genetic correlation with MDD and depressive symptoms (this genetic association is absent for cortical thickness 27 ), is determined earlier in development, and is less strongly affected by later environmental influences 71,79 .…”

Section: Cortical Thickness and Surface Areamentioning

confidence: 99%

ENIGMA MDD: seven years of global neuroimaging studies of major depression through worldwide data sharing

et al. 2020

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A key objective in the field of translational psychiatry over the past few decades has been to identify the brain correlates of major depressive disorder (MDD). Identifying measurable indicators of brain processes associated with MDD could facilitate the detection of individuals at risk, and the development of novel treatments, the monitoring of treatment effects, and predicting who might benefit most from treatments that target specific brain mechanisms. However, despite intensive neuroimaging research towards this effort, underpowered studies and a lack of reproducible findings have hindered progress. Here, we discuss the work of the ENIGMA Major Depressive Disorder (MDD) Consortium, which was established to address issues of poor replication, unreliable results, and overestimation of effect sizes in previous studies. The ENIGMA MDD Consortium currently includes data from 45 MDD study cohorts from 14 countries across six continents. The primary aim of ENIGMA MDD is to identify structural and functional brain alterations associated with MDD that can be reliably detected and replicated across cohorts worldwide. A secondary goal is to investigate how demographic, genetic, clinical, psychological, and environmental factors affect these associations. In this review, we summarize findings of the ENIGMA MDD disease working group to date and discuss future directions. We also highlight the challenges and benefits of largescale data sharing for mental health research.

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Mediation of the influence of childhood maltreatment on depression relapse by cortical structure: a 2-year longitudinal observational study

Cited by 115 publications

References 30 publications

Effect of Early Life Stress on the Epigenetic Profiles in Depression

Effect of Early Life Stress on the Epigenetic Profiles in Depression

Self-esteem and other risk factors for depressive symptoms among adolescents in United Arab Emirates

ENIGMA MDD: seven years of global neuroimaging studies of major depression through worldwide data sharing

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