Epigenetic Mechanisms in the Neurodevelopmental Theory of Depression.

Monika Talarowska

doi:10.1155/2020/6357873

Abstract

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?

Highlights

The genome, epigenome, and environment work together from the earliest stages of human life to create a specific phenotype of human health or disease (Figure 1)
The term “epigenetics” was first used by Waddington at the end of the 1930s to describe a phenomenon related to the fact that phenotypic changes do not always go hand in hand with genotype changes [1]
This paper will focus on issues related to mother–child interactions, making an attempt to demonstrate the influence of their epigenetic mechanisms leading in childhood and in adulthood to the occurrence of depressive symptoms [13]

Summary

Introduction

The genome (genes), epigenome (chemical modifications to DNA and chromatin), and environment work together from the earliest stages of human life to create a specific phenotype of human health or disease (Figure 1). Unique experiences for every human being, the history of growth, as well as interactions between genes and the environment—through epigenetic mechanisms—are considered to be a key mechanism triggering the symptoms of many somatic and mental diseases, including depression [9]. These gene–environment interactions cause epigenetic changes in gene expression patterns in which genes are switched to “on” or “off,” modifying the way cells function and affecting our predispositions for disease [10, 11]. This paper will focus on issues related to mother–child interactions, making an attempt to demonstrate the influence of their epigenetic mechanisms (mainly DNA methylation) leading in childhood and in adulthood to the occurrence of depressive symptoms [13]

Epigenetics in Depression

Depression

Oxytocin