Stress, epigenetics and depression: A systematic review

Park, Caroline; Rosenblat, Joshua D.; Brietzke, Elisa; Pan, Zihang; Lee, Yena; Cao, Bing; Zuckerman, Hannah; Kalantarova, Anastasia; McIntyre, Roger S.

doi:10.1016/j.neubiorev.2019.04.010

Cited by 267 publications

(153 citation statements)

References 59 publications

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“…Depression is a common mental disorder worldwide [1]. The pathogenesis of depression is not completely clear [2]. In addition to serotonin (5-HT) knowledge, immune activation and the production of inflammatory cytokines, such as IL-1β, IL-6, TNFα, are involved in depression because its symptomatology includes some behaviors that also occur during chronic inflammatory stress [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Proteomic profiling of the neurons in mice with depressive-like behavior induced by corticosterone and the regulation of berberine: pivotal sites of oxidative phosphorylation

et al. 2019

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Chronic corticosterone (CORT) stress is an anxiety and depression inducing factor that involves the dysfunction of glucocorticoid receptor (GR), brain-derived neurotrophic factor (BDNF), and neuronal plasticity. However, the regulation of proteomic profiles in neurons suffering CORT stress is remaining elusive. Thus, the proteomic profiles of mouse neuronal C17.2 stem cells were comprehensively investigated by TMT (tandem mass tag)-labeling quantitative proteomics. The quantitative proteomics conjugated gene ontology analysis revealed the inhibitory effect of CORT on the expression of mitochondrial oxidative phosphorylation-related proteins, which can be antagonized by berberine (BBR) treatment. In addition, animal studies showed that changes in mitochondria by CORT can affect neuropsychiatric activities and disturb the physiological functions of neurons via disordering mitochondrial oxidative phosphorylation. Thus, the mitochondrial energy metabolism can be considered as one of the major mechanism underlying CORT-mediated depression. Since CORT is important for depression after traumatic stress disorder, our study will shed light on the prevention and treatment of depression as well as posttraumatic stress disorder (PTSD).

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Section: Introductionmentioning

confidence: 99%

Proteomic profiling of the neurons in mice with depressive-like behavior induced by corticosterone and the regulation of berberine: pivotal sites of oxidative phosphorylation

et al. 2019

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“…Furthermore, research teams of Park et al [23] and Misra et al [24] have confirmed that stress-related epigenetic changes in the following genes: NRC31, SLCA4, BDNF, FKBP5, SKA2, OXTR, LINGO3, POU3F1, ID3, TPPP, GRIN1, and ITGB1 correlate with the occurrence of depression (respectively, Misra et al, [24]). Additionally, it has been noted that negative experiences from childhood, through epigenetic changes, may have a significant impact on the effectiveness of depression pharmacotherapy [25].…”

Section: Epigenetics In Depressionmentioning

confidence: 93%

“…The role of specific classes of long noncoding RNAs in resiliency or susceptibility to develop depression with a reciprocal response to antidepressant treatment is underlined [83]. Epigenetic changes in the signalling pathway of glucocorticosteroids (e.g., NR3C1, FKBP5), with regard to serotonergic neurotransmission (e.g., SLC6A4) and in the area of genes encoding neurotrophic factors (e.g., BDNF), seem to be the most promising therapeutic targets for future research [23,84].…”

Section: Further Directions Ofmentioning

confidence: 99%

Epigenetic Mechanisms in the Neurodevelopmental Theory of Depression

Talarowska

2020

Depression Research and Treatment

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The genome (genes), epigenome, and environment work together from the earliest stages of human life to produce a phenotype of human health or disease. Epigenetic modifications, including among other things: DNA methylation, modifications of histones and chromatin structure, as well as functions of noncoding RNA, are coresponsible for specific patterns of gene expression. This refers also to mental disorders, including depressive disorders. Early childhood experiences accompanied by severe stressors (considered a risk factor for depression in adult life) are linked with changes in gene expression. They include genes involved in a response to stress (hypothalamic-pituitary-adrenal axis, HPA), associated with autonomic nervous system hyperactivity and with cortical, and subcortical processes of neuroplasticity and neurodegeneration. These are, among others: gene encoding glucocorticoid receptor, FK506 binding protein 5 gene (FKBP5), gene encoding arginine vasopressin and oestrogen receptor alpha, 5-hydroxy-tryptamine transporter gene (SLC6A4), and gene encoding brain-derived neurotrophic factor. How about personality? Can the experiences unique to every human being, the history of his or her development and gene-environment interactions, through epigenetic mechanisms, shape the features of our personality? Can we pass on these features to future generations? Hence, is the risk of depression inherent in our biological nature? Can we change our destiny?

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“…maternal depression, malnutrition) has been associated with peripheral DNA methylation outcome later in life [ 18 ▪ , 20 , 22 – 24 ]. Although the studies in question are heterogenous with respect to methodology and results [ 18 ▪ , 23 ], available findings point to the potentials of epigenetic processes to constitute molecular mechanisms that could link environmental impacts, experienced at various moments throughout the life cycle (perinatal, childhood and adult) to mental-health outcomes, including eating disorders [ 8 , 18 ▪ , 23 ]. Importantly, methylation of some genes can also be altered by psychotherapeutic, nutritional or pharmacologic interventions [ 25 , 26 ▪▪ ], which raises the promise that changes in DNA methylation could serve as a marker for disease risk, staging, prognosis or therapeutic response.…”

Section: What Is Dna Methylation?mentioning

confidence: 99%

Applying epigenetic science to the understanding of eating disorders: a promising paradigm for research and practice

Booij

Steiger

2020

Current Opinion in Psychiatry

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Purpose of review Studies indicate that environmental factors, acting at various moments throughout the life cycle, can result in epigenetically mediated alterations in gene expression. In this article, we review recent findings on the role of epigenetic factors in eating disorders, address methodological issues that need to be considered when interpreting research findings, and comment on possible clinical applications. Recent findings Evidence suggests that eating disorders implicate alterations of methylation in genes involved in the mental status, metabolism, anthropometric features and immunity. Furthermore, some research in individuals with anorexia nervosa suggests the presence of reversible, malnutrition-induced epigenetic alterations that ‘reset’ as patients recover. Summary Epigenetic studies in the eating disorders corroborate the idea that eating disorder cause is multifactorial, and identify markers that could help inform our understanding of illness staging and subtyping that may explain the commonly progressive course of these disorders, and that may provide insights towards the development of novel interventions. Already, there is evidence to suggest that, in people with eating disorders, epigenetically informed interventions help reduce stigma and shame, and increase self-acceptance and hopes of recovery. Although findings are intriguing, further research is required as, to date, studies apply modest sample sizes and disparate methodologies.

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Stress, epigenetics and depression: A systematic review

Cited by 267 publications

References 59 publications

Proteomic profiling of the neurons in mice with depressive-like behavior induced by corticosterone and the regulation of berberine: pivotal sites of oxidative phosphorylation

Proteomic profiling of the neurons in mice with depressive-like behavior induced by corticosterone and the regulation of berberine: pivotal sites of oxidative phosphorylation

Epigenetic Mechanisms in the Neurodevelopmental Theory of Depression

Applying epigenetic science to the understanding of eating disorders: a promising paradigm for research and practice

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