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epigenetics & major depression

Shilpa Sharma, Ravi Shankar Akundi
BACKGROUND: Depression is a widespread phenomenon with varying degrees of pathology in different patients. Various hypotheses have been proposed for the cause and continuance of depression. Some of these include, but not limited to, the monoamine hypothesis, the neuroendocrine hypothesis, and the more recent epigenetic and inflammatory hypotheses. OBJECTIVE: In this article, we review all the above hypotheses with a focus on the role of mitochondria as the connecting link...
March 2, 2018: Current Neuropharmacology
Primoz Knap, Toma Tebaldi, Francesca Di Leva, Marta Biagioli, Mauro Dalla Serra, Gabriella Viero
Pathogenic bacteria produce powerful virulent factors, such as pore-forming toxins, that promote their survival and cause serious damage to the host. Host cells reply to membrane stresses and ionic imbalance by modifying gene expression at the epigenetic, transcriptional and translational level, to recover from the toxin attack. The fact that the majority of the human transcriptome encodes for non-coding RNAs (ncRNAs) raises the question: do host cells deploy non-coding transcripts to rapidly control the most energy-consuming process in cells-i...
November 3, 2017: Toxins
Paulina Misztak, Patrycja Pańczyszyn-Trzewik, Magdalena Sowa-Kućma
Major depressive disorder (MDD) represents approximately 40% of the disability caused by mental illnesses globally. The poorly understood pathophysiology and limited efficiency of pharmacological treatment (based primarily on the principles of the monoaminergic hypothesis) make depression a serious medical, public and socio-economical problem. An increasing number of studies suggest that epigenetic modifications (alterations in gene expression that are not due to changes in DNA sequence) in certain brain regions and neural circuits represent a key mechanism through which environmental factors interact with individual's genetic constitution to affect risk of mental disorders...
August 12, 2017: Pharmacological Reports: PR
Shile Qi, Xiao Yang, Liansheng Zhao, Vince D Calhoun, Nora Perrone-Bizzozero, Shengfeng Liu, Rongtao Jiang, Tianzi Jiang, Jing Sui, Xiaohong Ma
There is compelling evidence that epigenetic factors contribute to the manifestation of depression, in which microRNA132 (miR-132) is suggested to play a pivotal role in the pathogenesis and neuronal mechanisms underlying the symptoms of depression. Additionally, several depression-associated genes [MECP2, ARHGAP32 (p250GAP), CREB, and period genes] were experimentally validated as miR-132 targets. However, most studies regarding miR-132 in major depressive disorder are based on post-mortem, animal models or genetic comparisons...
February 2, 2018: Brain: a Journal of Neurology
Jun Wang, Georgia E Hodes, Hongxing Zhang, Song Zhang, Wei Zhao, Sam A Golden, Weina Bi, Caroline Menard, Veronika Kana, Marylene Leboeuf, Marc Xie, Dana Bregman, Madeline L Pfau, Meghan E Flanigan, Adelaida Esteban-Fernández, Shrishailam Yemul, Ali Sharma, Lap Ho, Richard Dixon, Miriam Merad, Ming-Hu Han, Scott J Russo, Giulio M Pasinetti
Major depressive disorder is associated with abnormalities in the brain and the immune system. Chronic stress in animals showed that epigenetic and inflammatory mechanisms play important roles in mediating resilience and susceptibility to depression. Here, through a high-throughput screening, we identify two phytochemicals, dihydrocaffeic acid (DHCA) and malvidin-3'-O-glucoside (Mal-gluc) that are effective in promoting resilience against stress by modulating brain synaptic plasticity and peripheral inflammation...
February 2, 2018: Nature Communications
Qingzhong Wang, Bhaskar Roy, Gustavo Turecki, Richard C Shelton, Yogesh Dwivedi
OBJECTIVE: Proinflammatory cytokines have recently received considerable attention for their role in suicidal behavior; however, how the expression of cytokine genes is regulated is not clearly known. The authors examined underlying mechanisms of critical cytokine gene tumor necrosis factor-alpha (TNF-α) dysregulation in the brains of individuals who died by suicide. METHOD: TNF-α expression was examined in the dorsolateral prefrontal cortex of the postmortem brains of persons with and without major depressive disorder who died by suicide and of persons with major depressive disorder who died of causes other than suicide...
January 24, 2018: American Journal of Psychiatry
Mihoko Shimada, Takeshi Otowa, Taku Miyagawa, Tadashi Umekage, Yoshiya Kawamura, Miki Bundo, Kazuya Iwamoto, Tempei Ikegame, Mamoru Tochigi, Kiyoto Kasai, Hisanobu Kaiya, Hisashi Tanii, Yuji Okazaki, Katsushi Tokunaga, Tsukasa Sasaki
Major depressive disorder is a common psychiatric disorder that is thought to be triggered by both genetic and environmental factors. Depressive symptoms are an important public health problem and contribute to vulnerability to major depression. Although a substantial number of genetic and epigenetic studies have been performed to date, the detailed etiology of depression remains unclear and there are no validated biomarkers. DNA methylation is one of the major epigenetic modifications that play diverse roles in the etiology of complex diseases...
January 5, 2018: Journal of Human Genetics
Peipei Wang, Qinyu Lv, Yemeng Mao, Cuizhen Zhang, Chenxi Bao, Hong Sun, Hanmei Chen, Zhenghui Yi, Weimin Cai, Yiru Fang
BACKGROUND: The serotonin receptor 1A and 1B (HTR1A/1B) gene have been suggested to be involved in the pathogenesis of major depressive disorder (MDD) and the antidepressant treatment response. Gene expression differences were partly mediated by genetic polymorphism and DNA methylation which might be affected by environmental factors. In the present study, we attempt to identify whether HTR1A/1B DNA methylation and genetic polymorphism could predict antidepressant treatment response. METHODS: 85 Chinese Han MDD patients were clinically assessed 8 weeks after of initiating escitalopram treatment for the first time...
December 7, 2017: Journal of Affective Disorders
Corina Nagy, Kathryn Vaillancourt, Gustavo Turecki
Chronic stressors, during developmental critical periods and beyond, contribute to the risk of developing psychiatric conditions, including major depressive disorder (MDD). Epigenetic mechanisms including DNA methylation and histone modifications, at key stress response and neurotrophin genes, are increasingly implicated in mediating this risk. Although the exact mechanisms through which stressful environmental stimuli alter the epigenome are still unclear, research from the learning and memory fields indicates that epigenomic marks can be altered, at least in part, through calcium-dependent signalling cascades in direct response to neuronal activity...
December 18, 2017: Genes, Brain, and Behavior
Benjamin Hing, Leela Sathyaputri, James B Potash
Major depressive disorder (MDD) is a mood disorder that affects behavior and impairs cognition. A gene potentially important to this disorder is the brain derived neurotrophic factor (BDNF) as it is involved in processes controlling neuroplasticity. Various mechanisms exist to regulate BDNF's expression level, subcellular localization, and sorting to appropriate secretory pathways. Alterations to these processes by genetic factors and negative stressors can dysregulate its expression, with possible implications for MDD...
December 15, 2017: American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics
Yosuke Yamawaki, Norika Yoshioka, Kanako Nozaki, Hikaru Ito, Keisuke Oda, Kana Harada, Satomi Shirawachi, Satoshi Asano, Hidenori Aizawa, Shigeto Yamawaki, Takashi Kanematsu, Hiroyuki Akagi
Patients with major depressive disorder have elevated peripheral inflammation; the degree of this increase correlates with the severity of the disorder. Chronic psychological stress increases pro-inflammatory cytokines and promotes microglial activation, leading to stress vulnerability. Epigenetics, including DNA methylation and histone modification, are also related to the pathophysiology of major depressive disorder. Sodium butyrate (SB), a histone deacetylase inhibitor, exerts an antidepressant effect by altering gene expression in the hippocampus...
February 1, 2018: Brain Research
Leonardo Tozzi, Chloe Farrell, Linda Booij, Kelly Doolin, Zsofia Nemoda, Moshe Szyf, Florence B Pomares, Julian Chiarella, Veronica O'Keane, Thomas Frodl
The gene for the glucocorticoid receptor regulator FK506 binding protein 5 (FKBP5) plays a role for risk, response to treatment, and changes in brain areas in major depressive disorder (MDD). Chronic stress is associated with lower methylation of FKBP5. Our aim was to investigate whether methylation of FKBP5 reflected exposure to childhood adversity in MDD and controls and whether it was associated with structure and function of emotional processing regions. FKBP5 intron 7 GR response element region methylation and rs1360780 allelic status were assessed from whole blood in 56 MDD adults and 50 controls...
November 28, 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
Stephanie H Parade, Andrew M Novick, Justin Parent, Ronald Seifer, Samantha J Klaver, Carmen J Marsit, Asi Polly Gobin, Bao-Zhu Yang, Audrey R Tyrka
Serotonin signaling pathways play a key role in brain development, stress reactivity, and mental health. Epigenetic alterations in the serotonin system may underlie the effect of early life stress on psychopathology. The current study examined methylation of the serotonin receptor 2A (HTR2A) gene in a sample of 228 children including 119 with child welfare documentation of moderate to severe maltreatment within the last 6 months. Child protection records, semistructured interviews in the home, and parent reports were used to assess child stress exposure, psychiatric symptoms, and behavior...
December 2017: Development and Psychopathology
Shusaku Uchida, Hirotaka Yamagata, Tomoe Seki, Yoshifumi Watanabe
Major depressive disorder is one of the most common mental illnesses as it affects more than 350 million people globally. Major depressive disorder is etiologically complex and disabling. Genetic factors play a role in the etiology of major depression. However, identical twin studies have shown high rates of discordance, indicating non-genetic mechanisms as well. For instance, stressful life events increase the risk of depression. Environmental stressors also induce stable changes in gene expression within the brain that may lead to maladaptive neuronal plasticity in regions implicated in disease pathogenesis...
November 20, 2017: Psychiatry and Clinical Neurosciences
Mario F Juruena, Mariia Bocharova, Bruno Agustini, Allan H Young
BACKGROUND: The link between the abnormalities of the Hypothalamic-pituitary-adrenal (HPA) axis and depression has been one of the most consistently reported findings in psychiatry. At the same time, multiple studies have demonstrated a stronger association between the increased activation of HPA-axis and melancholic, or endogenous depression subtype. This association has not been confirmed for the atypical subtype, and some researchers have suggested that as an antinomic depressive subtype, it may be associated with the opposite type, i...
October 6, 2017: Journal of Affective Disorders
Naohiro Takeuchi, Shinpei Nonen, Masaki Kato, Masataka Wakeno, Yoshiteru Takekita, Toshihiko Kinoshita, Fumihiko Kugawa
BACKGROUND: Antidepressants have variable therapeutic effects, depending on genetic and environmental factors. Approximately 30% of major depressive disorder (MDD) patients do not respond significantly to antidepressants such as paroxetine, a selective serotonin reuptake inhibitor (SSRI). However, the biological mechanisms behind this phenomenon are mostly unknown. Here, we examined the role of patients' epigenetic background in SSRI efficacy. METHODS: Genome-wide DNA methylation analysis of the peripheral blood of Japanese MDD patients was performed by using the Infinium HumanMethylation450 BeadChip...
November 4, 2017: Neuropsychobiology
Massimiliano Buoli, Marta Serati, Silvia Grassi, Laura Pergoli, Laura Cantone, A Carlo Altamura, Valentina Bollati
BACKGROUND: Circadian rhythms are largely dysregulated in Major Depressive Disorder (MDD). The present review provides a summary of the findings about the role of clock genes in the etiology of MDD. METHODS: A careful search of articles on Pubmed, PsycINFO, Isi Web of Knowledge was performed in order to obtain a comprehensive review about the topic. RESULTS: The studies reported contrasting results about the association of different single nucleotide polymorphisms (SNPs) in clock genes and MDD...
November 7, 2017: Journal of Affective Disorders
Ilona Schneider, Harald Kugel, Ronny Redlich, Dominik Grotegerd, Christian Bürger, Paul-Christian Bürkner, Nils Opel, Katharina Dohm, Dario Zaremba, Susanne Meinert, Nina Schröder, Anna Milena Straßburg, Kathrin Schwarte, Christiane Schettler, Oliver Ambrée, Stephan Rust, Katharina Domschke, Volker Arolt, Walter Heindel, Bernhard T Baune, Weiqi Zhang, Udo Dannlowski, Christa Hohoff
DNA methylation profiles of the serotonin transporter gene (SLC6A4) have been shown to alter SLC6A4 expression, drive antidepressant treatment response and modify brain functions. This study investigated whether methylation of an AluJb element in the SLC6A4 promotor was associated with major depressive disorder (MDD), amygdala reactivity to emotional faces, 5-HTTLPR/rs25531 polymorphism, and recent stress. MDD patients (n=122) and healthy controls (HC, n=176) underwent fMRI during an emotional face-matching task...
November 7, 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
Katherine McEvoy, Lauren M Osborne, Julie Nanavati, Jennifer L Payne
PURPOSE OF REVIEW: The purpose of this study is to review and summarize the literature exploring the genetic basis for premenstrual dysphoric disorder (PMDD) and postpartum depression (PPD). RECENT FINDINGS: There is more evidence for a genetic basis for PPD than for PMDD, but only when PPD is defined as beginning in the immediate postpartum time period. Familial, genome-wide linkage and association studies, and candidate gene studies, most in the past 10 years, have examined the genetic etiology of reproductive affective disorders, including PMDD and PPD...
October 30, 2017: Current Psychiatry Reports
Joanne Ryan, Lauren Pilkington, Katharina Neuhaus, Karen Ritchie, Marie-Laure Ancelin, Richard Saffery
BACKGROUND: It is well established that there is a link between inflammation and depression, with several studies reporting increased circulating levels of the pro-inflammatory cytokine, interleukin-6 (IL6), in depressed individuals. Peripheral epigenetic marks, including DNA methylation, hold promise as biomarkers for a range of complex conditions, with potential to inform diagnosis and tailor interventions. The aim of this study was to determine whether individuals with depression display differential methylation of the IL6 gene promoter compared to individuals without depression...
October 25, 2017: BMC Psychiatry
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