The neurobiological effects of stress as contributors to psychiatric disorders: focus on epigenetics

Provençal, Nadine; Binder, Elisabeth B.

doi:10.1016/j.conb.2014.08.007

Cited by 57 publications

(37 citation statements)

References 59 publications

(57 reference statements)

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“…Most work on mental health and epigenetics is in adults, but some work involving children is beginning to emerge (84,85). A growing literature shows that epigenetic patterns are related to depression and depressive-like symptoms, but these are often cross-sectional studies (86,87).…”

Section: Epigenetics and Children’s Healthmentioning

confidence: 99%

DNA methylation, early life environment, and health outcomes

2015

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Epigenetics, and especially DNA methylation, have recently become provocative biological explanations for early-life environmental effects on later health. Despite the large increase in papers on the topic over the last few years, many questions remain with regards to the biological feasibility of this mechanism and the strength of the evidence to date. In this review, we examine the literature on early-life effects on epigenetic patterns, with special emphasis on social environmental influences. First, we review the basic biology of epigenetic modification of DNA and debate the role of early-life stressful, protective, and positive environments on gene-specific, system-specific, and whole-genome epigenetic patterns later in life. Second, we compare the epigenetic literatures of both humans and other animals and review the research linking epigenetic patterns to health in order to complete the mechanistic pathway. Third, we discuss physical environmental and social environmental effects, which have to date, generally not been jointly considered. Finally, we close with a discussion of the current state of the area’s research, its future direction, and its potential use in pediatric health.

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Section: Epigenetics and Children’s Healthmentioning

confidence: 99%

DNA methylation, early life environment, and health outcomes

2015

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“…PTSD arises from interactions between traumatic stresses and various genetic factors (Skelton et al, 2012). Epigenetic alterations are thought to be the core causes of these interactions, mediating the continuing effects of the environment on gene regulation (Provencal and Binder, 2015;Zannas et al, 2015). Many studies in both humans and animals have suggested that the epigenetic regulation of distinct genes play roles in the pathogenesis of PTSD (Labonté et al, 2014;Byun et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic mechanism of maternal post-traumatic stress disorder in delayed rat offspring development: dysregulation of methylation and gene expression

X-G

Zhang

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Maternal post-traumatic stress disorder (PTSD) increases the risk of adverse neurodevelopmental outcomes in the child. Epigenetic alternations may play an essential role in the negative effects of PTSD. This study was aimed to investigate the possible epigenetic alterations of maternal PTSD, which underpins the developmental and behavioral impact. 24 pregnant Sprague-Dawley (SD) rats were randomly grouped into PTSD and control groups. Open-field tests (OFTs), elevated pull maze (EPM) assays, gene expression profile chip tests, and methylated DNA immunoprecipitation sequencing (MeDIPSeq) were performed on the offsprings 30 days after birth. The results 2 X.G. Zhang et al. Genetics and Molecular Research 15 (3): gmr.15039009 showed that PTSD offsprings had lower body weights and OFT scores than control offsprings. Enzyme-linked immunosorbent assays showed that serotonin receptor (5-HT) and dopamine levels were significantly lower in PTSD offsprings than in control offsprings. In contrast, corticosterone levels were higher in the PTSD group than in the control group. In a comparison of the PTSD group versus the control group, 4,160 significantly differentially methylated loci containing 30,657 CpGs were identified; 2,487 genes, including 13 dysmethylated genes, were validated by gene expression profiling, showing a negative correlation between methylation and gene expression (R = -0.617, P = 0.043). In conclusion, maternal PTSD could delay the physical and behavioral development of offsprings, and the underlying mechanism could contribute to changes in neurotransmitters and gene expression, owing to dysregulation of wholegenome methylation. These findings could support further clinical research on appropriate interventions for maternal PTSD to prevent methylation dysregulation and developmental retardation.

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“…Personality factors have been from the earliest descriptions of vascular depression considered to be defining components of a clinical model for this entity, but translation of neuropsychological dimensions into recognizable vignettes can be problematic . One broad interpretation of the personality‐related findings in vascular depression is that they induce or exacerbate stress, and stress itself entails adverse neurobiological consequences . Queen Victoria's brooding Journal entries over the 5‐month span of her second depression might then be understood as reflecting a stressful activation of her emotive personality style, with exacerbating effects on the expression of her mood symptoms.…”

Section: Discussionmentioning

confidence: 99%

“…18,19 One broad interpretation of the personality-related findings in vascular depression is that they induce or exacerbate stress, and stress itself entails adverse neurobiological consequences. 20 Queen Victoria's brooding Journal entries over the 5-month span of her second depression might then be understood as reflecting a stressful activation of her emotive personality style, with exacerbating effects on the expression of her mood symptoms.…”

Section: The Clinical Modelmentioning

confidence: 99%

Vascular depression and the death of Queen Victoria

Abrams

Alexopoulos

2018

Int J Geriat Psychiatry

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Objectives The aim of this article was to examine relationships between the neurological events that were the immediate cause of the death of Queen Victoria and the late‐life depression that preceded it. Methods/Design The authors closely reviewed the surviving medical notes of Queen Victoria's personal physician, Sir James Reid,Bt. recorded during the Queen's last 10 days of life. These notes were summarized in a chronological narrative and their implications considered in light of current concepts of vascular depression. Results The depression that Queen Victoria experienced over the 5 months prior to her death and during her final 10 days from 13 January 1901 until 22 January likely had a vascular etiology. Conclusions Although conclusions from this study are necessarily speculative given the lack of neuroimaging and other diagnostic tools available in 1901, it emerged that Queen Victoria had experienced early‐onset depression followed in later life by an acute depressive episode associated with vascular risk factors and personal losses, a sequence also encountered by today's geriatricians. In addition, etiological connections between the Queen's early‐onset and late‐life depressions appeared probable. Underlined for contemporary practitioners are the suffering experienced by patients with vascular depression at the end of their lives, as well as the struggles of physicians like Sir James Reid to provide clinical wisdom and emotional support.

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The neurobiological effects of stress as contributors to psychiatric disorders: focus on epigenetics

Cited by 57 publications

References 59 publications

DNA methylation, early life environment, and health outcomes

DNA methylation, early life environment, and health outcomes

Epigenetic mechanism of maternal post-traumatic stress disorder in delayed rat offspring development: dysregulation of methylation and gene expression

Vascular depression and the death of Queen Victoria

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