Journal of Child and Adolescent Behavior
Open Access

Epigenetic; DNA Methylation; MicroRNA; Histone Modification; Depression; Acute Depression; Chronic Depression; Early Childhood Depression; Traumatic Depression; Suicide

Introduction

The field of epigenetics has gained importance in recent years. Determining the repertoire of epigenetic changes that occur in the genome after depression not only provides insight into the temporal effects of depression on an individual’s biology, but also has valuable implications for an individual’s future response to depression also provide information. The term epigenetics has been used by Berger defined “A stably heritable phenotype resulting from a chromosomal change that is not accompanied by a change in the DNA sequence”. Epigenetic changes are known to be somatically transmitted from cell to cell, and in some cases, to be inherited across generations, indicating that epigenetic changes occur even in the absence of inhibitors also means that it will persist to the next generation. Berger they further subdivided epigenetics into three categories: “epigenators,” environmental triggers that affect cellular processes within cells, and “initiators,” intracellular signals that affect the epigenome and local histones, which we call “maintainers.” DNA methylation that maintains mutation and chromatin state. Epigenators are upstream signals from the environment or other signaling pathways that activate initiators. An example of this has been demonstrated by Cheeseman and Weitzman using Apicomplexa strain parasites and their proteomes that function as epigenators in putative pathogenesis. The initiator then interprets the signal to identify the exact place to trade. This locus may contain DNA, non-coding RNA, histones and other structures involved in chromatin remodeling. Maintainers support an ‘epigenetic chromatin state’ at specific sites through DNA methylation and other specific epigenetic modifications [1].

Epigenetic modifications include DNA methylation, noncoding RNAs such as microRNAs, histone modifications by methylation, acetylation, ubiquitination, phosphorylation, and other modifications such as SUMOylation. DNA methylation is performed by enzymes known as DNA methyltransferases, which transfer methyl groups to Cytosine Guanine Dinucleotide (CpG) regions of DNA. DNA methylation patterns correlate with levels of gene expression, particularly transcription reduction. Histone modifications occur through arginine methylation or lysine acetylation as in DNA, resulting in chromosome condensation or opening. Non-coding RNAs are RNA molecules that do not code for proteins, but support other functions. Examples of non-coding RNAs are microRNAs (miRNAs). miRNAs can interact with genetic material such as mRNA in ways that regulate gene expression. These epigenetic changes are subject to a variety of external influences, ranging from different types of depression, diet, lifestyle and environment. The persistence of these markers is a subject of much research and is still being investigated [2].

A healthy physiological response to depression is designed to maintain homeostasis and survival. Upon recognition of depression, the Hypothalamic-Pituitary-Adrenal (HPA) axis is activated by the paraventricular nucleus of the hypothalamus to release Corticotropin- Releasing Hormone (CTRH), which leads to the anterior pituitary lobe activated to release Adreno Corticotropic Hormone (ACTH). ACTH works on the adrenal glands by releasing glucocorticoids such as cortisol. Cortisol exerts a systemic effect on the site of the glucocorticoid receptor (Nr3c1) and adversely affects the hypothalamus and anterior pituitary, releasing their respective inhibitory hormones. Increased CTRH release alters the rhythmic and pulsatile nature of CTRH release when depression occurs. Depression has also been shown to impair the immune system. As reported by Dragos Studies have shown that acute depression enhances resistance to infections, whereas chronic depression weakens resistance to infections. Furthermore, a study conducted in subjects with acute traumatic brain injury showed an inverse correlation between circulating immune T cells and plasma cortisol levels in mice [3].

Depression is an inevitable part of life. This review will focus on his five categories of different types of depression and their associated epigenetic alterations. Depending on the type of depression an individual is experiencing, depression may function within human cells as an epigenerator, causing initiator-induced changes and stabilizing epigenetic changes through maintainer activity can cause it. There are different types of depression epigenators, including acute depression, chronic depression, childhood depression, traumatic depression, and suicide. Acute depression is defined as short-term events that cause depression in a person, or events that mimic acute events. Chronic depression is defined as an event that occurs over a period of time or an experiment that mimics chronic depression or chronic depression in a person. Depression that occurs during puberty is considered infantile depression, but does not include utero-maternal depression. Traumatic depression is defined as an event that has a frightening, dangerous, and/ or shocking effect and that has either acute depressive disorder or Post- Traumatic Depressive Disorder (PTSD), or post-exposure Defined as events that are highly correlated with the development of these disorders. Suicide is defined as either the thought of ending one’s life, the attempted suicide, or the completion of such an act [4].

Discussion

Acute Depression

Acute depression is defined as an event in which a person becomes depressed for a short period of time and then subsides. To assess the effects of acute depression, researchers in the literature used tests ranging from acute exposure to benzo[a]pyrene and ultraviolet light to restraint tests, febrile depression, and the Trier Social Depression Test (TSST). I’ve been testing in different ways for psychosocial depression and swimming tests. In experiments with red mussel gills, showed that acute exposure to benzo[a]pyrene, a compound found in cigarette smoke, coal, and tar, resulted in a reduction in global DNA methylation levels. , suggest that short-term exposure to chemical inhibitors such as benzo[a]pyrene can potentially cause the following symptoms: Epigenetic changes in model organisms. In addition to these findings, recent literature indicates that a subset of immune cells (lymphocytes) may be potential predictors of genome-wide DNA methylation. In a study of adults with acute psychosocial depression, Apsley showed an increase in immune cells and concomitant increases in genome-wide DNA methylation changes.

A key receptor in the depression response is the glucocorticoid receptor. Without these, model organisms (such as mice and humans) lack receptor binding and cannot elicit a full response to depression. It can cause brain disorders such as depression. Different studies have examined methylation changes in different regions of the glucocorticoid receptor gene (Nr3c1). His 3′UTR region of Nr3c1 5-hydroxymethylcytosine (5-hmC) is altered by acute restraint inhibition tests. They found that hippocampal depression in male mice increased his 5-hmC in the 3’UTR region. A second group of scientists, found 1-C in the Nr3c1 gene in human participants (N = 675) resulting from three different psychosocial depressions, including language tests, mirror tracking tests, and Stroop tests. They observed that decreased depressive reactivity as measured by heart rate and cortisol response was associated with decreased levels of methylation in the 1-C promoter region in fasting blood samples. However, when these results were adjusted for lifestyle variables such as gender and smoking, the association dissipated, suggesting that lifestyle differences played a greater role. Interestingly, lower levels of methylation in the promoter region 1-C of the Nr3c1 gene were associated with greater perception of depression and lower perceived control and performance. A third group of scientists and colleagues, focused on a region upstream of exon 2 of the Nr3c1 gene, called ‘GR area 1’, and a region around exon 17 called ‘GR area 2’ in the hippocampus of male [5].

His CpG values in ‘GR area 1’ were not affected by the dentate gyrus or the ammonia angle, whereas in ‘GR area 2’ there was a significant increase in methylation in the dentate gyrus based on the swim suppression test. A decrease in the ammonia angle was shown. Studies of epigenetic changes along the Nr3c1 gene between human and animal studies have revealed variable region alterations that reflect various acute depressive factors applied [6].

Chronic Depression

Chronic depression is defined as recurrent or long-term exposure to depression. In animal models, chronic restraint tests, forced swimming tests at different water temperatures on consecutive days, chronic water avoidance, contact with other animals, and social defeat tests are common methods of testing for chronic depression. . In human subjects, the effects of chronic depression are determined by the workplace, living situation, high-altitude platform, and participants’ exposure to chronic depression in the chronic social defeat test. Studies examining epigenetic changes in chronic depression have been performed and observed in mice, rats, and humans. McEwen outlines the effects of chronic depression on the whole body, emphasizing that chronic depression can lead to profound changes in the brain, causing neural imbalances. These large-scale changes can also lead to behavioral changes. A possible cause of this imbalance could be the influence of epigenetics on the generation X environment model [7].

Early Childhood Depression

Trauma experienced early in life, occurring only at specific developmental stages throughout life, is commonly referred to in the research literature as ACE (Adverse Childhood Experience), ELE (Early Life Depression), or CM (Childhood Maltreatment). Examples of early childhood trauma include physical, sexual, or emotional abuse or neglect, domestic violence, or a hostile social environment (eg, violence). B. Bullying. A number of studies suggest that early traumatic experiences are associated with epigenomic alterations and are also associated with impaired brain developmental programs, psychiatric disorders, and increased risk of substance abuse and suicide. In addition to psychiatric disorders, childhood trauma is also highly correlated with adverse physical health effects such as metabolic syndrome, chronic pain, and increased cancer risk. It has been shown that the molecular changes triggered by such episodes of negative childhood experiences depend on individual genetics, type of depression, and timing of depression, suggesting that previous depression experience May be associated with long-term effects. Overall, in both animal and human studies early in life in response to depression, differentially methylated gene and intergenic regions of the genome compared with those who had not experienced childhood trauma reported changes in changes miRNA levels in response to depression, and different global methylation patterns [8].

Conclusion

Given that various forms of depression cause specific epigenetic changes and that these changes are associated with worsening psychiatric and physiological health, intentional reversal of these signs may help patients hope to improve outcomes for they studied the role of exercise in positively affecting patients suffering from various depressions, such as cancer and neurodegenerative diseases, through epigenetic mechanisms. Furthermore, have shown that exercise mimics the acute depressive response in the hippocampus of mice and increases BDNF mRNA levels, observed immediately after acute depression by histone H3 acetylation of the promoter region of BDNF shown to prevent its decline. Additionally, yoga has been shown to have some changes in DNA methylation patterns and proteins involved in immunity. The opportunity to prevent or modify the methylation pathway induced by depression overload. A pilot study conducted in veterans with PTSD showed that some psychotherapies may provide epigenetic solutions to methylation changes in the Nr3c1 and FKBP5 genes. However, the results were not statistically significant and require further validation. Furthermore, a pilot study investigating the mechanism of MDMA’s efficacy in treating PTSD found that patients who responded to MDMA treatment exhibited greater methylation changes at one site in the NR3C1 gene compared to placebo. Results obtained from both narrative exposure therapy and MDMA interventions highlight the need for individualized medical approaches to treat patients with trauma-related disorders. Additionally, some of the current highlights in the meditation literature were discussed as offering ways to prevent or reverse the effects of environmental suppression. However, researchers debate the unclear nature of the molecular basis of meditation and whether it acts at the same epigenetic sites or through different mechanisms. This highlights a potential gap in the literature. Taken together, this nonexhaustive list of possible non-pharmacological ‘solutions’ may offer opportunities to inhibit and even reverse epigenetic changes that occur during the course of a person’s life experiences [9, 10].

Acknowledgement

None

Conflict of Interest

None

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