Relevant bibliographies by topics / Epigenetic disorders

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Academic literature on the topic 'Epigenetic disorders'

Author: Grafiati
Published: 24 April 2022

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Journal articles on the topic "Epigenetic disorders"

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Tran, Nguyen Quoc Vuong, and Kunio Miyake. "Neurodevelopmental Disorders and Environmental Toxicants: Epigenetics as an Underlying Mechanism." International Journal of Genomics 2017 (2017): 1–23. http://dx.doi.org/10.1155/2017/7526592.

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The increasing prevalence of neurodevelopmental disorders, especially autism spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD), calls for more research into the identification of etiologic and risk factors. The Developmental Origin of Health and Disease (DOHaD) hypothesizes that the environment during fetal and childhood development affects the risk for many chronic diseases in later stages of life, including neurodevelopmental disorders. Epigenetics, a term describing mechanisms that cause changes in the chromosome state without affecting DNA sequences, is suggested to be the underlying mechanism, according to the DOHaD hypothesis. Moreover, many neurodevelopmental disorders are also related to epigenetic abnormalities. Experimental and epidemiological studies suggest that exposure to prenatal environmental toxicants is associated with neurodevelopmental disorders. In addition, there is also evidence that environmental toxicants can result in epigenetic alterations, notably DNA methylation. In this review, we first focus on the relationship between neurodevelopmental disorders and environmental toxicants, in particular maternal smoking, plastic-derived chemicals (bisphenol A and phthalates), persistent organic pollutants, and heavy metals. We then review studies showing the epigenetic effects of those environmental factors in humans that may affect normal neurodevelopment.
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Kubota, T., K. Miyake, N. Hariya, and K. Mochizuki. "Understanding the epigenetics of neurodevelopmental disorders and DOHaD." Journal of Developmental Origins of Health and Disease 6, no. 2 (February 24, 2015): 96–104. http://dx.doi.org/10.1017/s2040174415000057.

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The Developmental Origins of Health and Disease (DOHaD) hypothesis refers to the concept that ‘malnutrition during the fetal period induces a nature of thrift in fetuses, such that they have a higher change of developing non-communicable diseases, such as obesity and diabetes, if they grow up in the current well-fed society.’ Epigenetics is a chemical change in DNA and histones that affects how genes are expressed without alterations of DNA sequences. Several lines of evidence suggest that malnutrition during the fetal period alters the epigenetic expression status of metabolic genes in the fetus and that this altered expression can persist, and possibly lead to metabolic disorders. Similarly, mental stress during the neonatal period can alter the epigenetic expression status of neuronal genes in neonates. Moreover, such environmental, stress-induced, epigenetic changes are transmitted to the next generation via an acquired epigenetic status in sperm. The advantage of epigenetic modifications over changes in genetic sequences is their potential reversibility; thus, epigenetic alterations are potentially reversed with gene expression. Therefore, we potentially establish ‘preemptive medicine,’ that, in combination with early detection of abnormal epigenetic status and early administration of epigenetic-restoring drugs may prevent the development of disorders associated with the DOHaD.
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La Rovere, Marina, Marica Franzago, and Liborio Stuppia. "Epigenetics and Neurological Disorders in ART." International Journal of Molecular Sciences 20, no. 17 (August 26, 2019): 4169. http://dx.doi.org/10.3390/ijms20174169.

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About 1–4% of children are currently generated by Assisted Reproductive Technologies (ART) in developed countries. These babies show only a slightly increased risk of neonatal malformations. However, follow-up studies have suggested a higher susceptibility to multifactorial, adult onset disorders like obesity, diabetes and cardiovascular diseases in ART offspring. It has been suggested that these conditions could be the consequence of epigenetic, alterations, due to artificial manipulations of gametes and embryos potentially able to alter epigenetic stability during zygote reprogramming. In the last years, epigenetic alterations have been invoked as a possible cause of increased risk of neurological disorders, but at present the link between epigenetic modifications and long-term effects in terms of neurological diseases in ART children remains unclear, due to the short follow up limiting retrospective studies. In this review, we summarize the current knowledge about neurological disorders promoted by epigenetics alterations in ART. Based on data currently available, it is possible to conclude that little, if any, evidence of an increased risk of neurological disorders in ART conceived children is provided. Most important, the large majority of reports appears to be limited to epidemiological studies, not providing any experimental evidence about epigenetic modifications responsible for an increased risk.
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Blacker, Caren J., Mark A. Frye, Eva Morava-Kozicz, Tamas Kozicz, and Marin Veldic. "A Review of Epigenetics of PTSD in Comorbid Psychiatric Conditions." Genes 10, no. 2 (February 13, 2019): 140. http://dx.doi.org/10.3390/genes10020140.

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Post-traumatic stress disorder (PTSD) is an acquired psychiatric disorder with functionally impairing physiological and psychological symptoms following a traumatic exposure. Genetic, epigenetic, and environmental factors act together to determine both an individual’s susceptibility to PTSD and its clinical phenotype. In this literature review, we briefly review the candidate genes that have been implicated in the development and severity of the PTSD phenotype. We discuss the importance of the epigenetic regulation of these candidate genes. We review the general epigenetic mechanisms that are currently understood, with examples of each in the PTSD phenotype. Our focus then turns to studies that have examined PTSD in the context of comorbid psychiatric disorders or associated social and behavioral stressors. We examine the epigenetic variation in cases or models of PTSD with comorbid depressive disorders, anxiety disorders, psychotic disorders, and substance use disorders. We reviewed the literature that has explored epigenetic regulation in PTSD in adverse childhood experiences and suicide phenotypes. Finally, we review some of the information available from studies of the transgenerational transmission of epigenetic variation in maternal cases of PTSD. We discuss areas pertinent for future study to further elucidate the complex interactions between epigenetic modifications and this complex psychiatric disorder.
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Duan, Yong-Tao, Chetan B. Sangani, Wei Liu, Kunjal V. Soni, and Yongfang Yao. "New Promises to Cure Cancer and Other Genetic Diseases/Disorders: Epi-drugs Through Epigenetics." Current Topics in Medicinal Chemistry 19, no. 12 (July 30, 2019): 972–94. http://dx.doi.org/10.2174/1568026619666190603094439.

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All the heritable alterations in gene expression and chromatin structure due to chemical modifications that do not involve changes in the primary gene nucleotide sequence are referred to as epigenetics. DNA methylation, histone modifications, and non-coding RNAs are distinct types of epigenetic inheritance. Epigenetic patterns have been linked to the developmental stages, environmental exposure, and diet. Therapeutic strategies are now being developed to target human diseases such as cancer with mutations in epigenetic regulatory genes using specific inhibitors. Within the past two decades, seven epigenetic drugs have received regulatory approval and many others show their candidature in clinical trials. The current article represents a review of epigenetic heritance, diseases connected with epigenetic alterations and regulatory approved epigenetic drugs as future medicines.
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Martínez-Iglesias, Olaia, Vinogran Naidoo, Natalia Cacabelos, and Ramón Cacabelos. "Epigenetic Biomarkers as Diagnostic Tools for Neurodegenerative Disorders." International Journal of Molecular Sciences 23, no. 1 (December 21, 2021): 13. http://dx.doi.org/10.3390/ijms23010013.

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Epigenetics is the study of heritable changes in gene expression that occur without alterations to the DNA sequence, linking the genome to its surroundings. The accumulation of epigenetic alterations over the lifespan may contribute to neurodegeneration. The aim of the present study was to identify epigenetic biomarkers for improving diagnostic efficacy in patients with neurodegenerative diseases. We analyzed global DNA methylation, chromatin remodeling/histone modifications, sirtuin (SIRT) expression and activity, and the expression of several important neurodegeneration-related genes. DNA methylation, SIRT expression and activity and neuregulin 1 (NRG1), microtubule-associated protein tau (MAPT) and brain-derived neurotrophic factor (BDNF) expression were reduced in buffy coat samples from patients with neurodegenerative disorders. Our data suggest that these epigenetic biomarkers may be useful in clinical practical for the diagnosis, surveillance, and prognosis of disease activity in patients with neurodegenerative diseases.
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Tzouvelekis, Argyrios, and Naftali Kaminski. "Epigenetics in idiopathic pulmonary fibrosis." Biochemistry and Cell Biology 93, no. 2 (April 2015): 159–70. http://dx.doi.org/10.1139/bcb-2014-0126.

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Idiopathic pulmonary fibrosis (IPF) is a lethal chronic lung disorder with no effective treatment and a prognosis worse than that of lung cancer. Despite extensive research efforts, its etiology and pathogenesis still remain largely unknown. Current experimental evidence has shifted the disease paradigm from chronic inflammation towards the premise of abnormal epithelial wound repair in response to repeated epigenetic injurious stimuli in genetically predisposed individuals. Epigenetics is defined as the study of heritable changes in gene function by factors other than an individual’s DNA sequence, providing valuable information regarding adaption of genes to environmental changes. Although cancer is the most studied disease with relevance to epigenetic modifications, recent data support the idea that epigenomic alterations may lead to variable disease phenotypes, including fibroproliferative lung disorders such as IPF. This review article summarizes the latest experimental and translational epigenetic studies in the research field of chronic lung disorders, mainly focusing on IPF, highlights current methodology limitations, and underlines future directions and perspectives.
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Kundakovic, Marija. "Prenatal Programming of Psychopathology: The Role of Epigenetic Mechanisms / PRENATALNO PROGRAMIRANJE PSIHIJATRIJSKIH POREMEĆAJA: ULOGA EPIGENETSKIH MEHANIZAMA." Journal of Medical Biochemistry 32, no. 4 (October 1, 2013): 313–24. http://dx.doi.org/10.2478/jomb-2013-0047.

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Summary The Human Genome Project, completed ten years ago, widely opened the door for the field of Epigenetics as a new venue to study the causes of human disease and to search for predictive biomarkers and therapeutic targets for a wide range of disorders. The field of behavioral and psychiatric epigenetics is still very young, but increasing evidence suggests that epigenetic mechanisms contribute to the development of neuropsychiatric disorders. The prenatal period is particularly vulnerable to epigenetic disruption, and it seems likely that adverse in utero environments can induce epigenetic dysregulation and predispose an individual to mental disease later in life. Emerging evidence from animal studies has shown that maternal exposure to drugs, stress, and toxicants can alter epigenetic gene programming in the brain and contribute to neurodevelopmental and behavioral deficits in the offspring. The evidence from human studies is more limited but is in agreement with animal data. Several human studies have shown that prenatal risk factors, such as maternal food deprivation and stressful life events, are associated with persistent epigenetic changes in genes that are linked to neurodevelopmental disorders and psychopathology. Although these studies support the hypothesis that epigenetic mechanisms may be involved in prenatal programming of psychopathology, a collaborative effort of basic, clinical and epidemiological research is needed to advance this field. Nevertheless, this field holds great promise to facilitate our understanding of environmental contribution to human mental disease and to reveal new predictive biomarkers as well as preventive and therapeutic approaches for various neuropsychiatric disorders.
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Wang, Tian, Jie Zhang, and Yi Xu. "Epigenetic Basis of Lead-Induced Neurological Disorders." International Journal of Environmental Research and Public Health 17, no. 13 (July 7, 2020): 4878. http://dx.doi.org/10.3390/ijerph17134878.

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Environmental lead (Pb) exposure is closely associated with pathogenesis of a range of neurological disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), attention deficit/hyperactivity disorder (ADHD), etc. Epigenetic machinery modulates neural development and activities, while faulty epigenetic regulation contributes to the diverse forms of CNS (central nervous system) abnormalities and diseases. As a potent epigenetic modifier, lead is thought to cause neurological disorders through modulating epigenetic mechanisms. Specifically, increasing evidence linked aberrant DNA methylations, histone modifications as well as ncRNAs (non-coding RNAs) with AD cases, among which circRNA (circular RNA) stands out as a new and promising field for association studies. In 23-year-old primates with developmental lead treatment, Zawia group discovered a variety of epigenetic changes relating to AD pathogenesis. This is a direct evidence implicating epigenetic basis in lead-induced AD animals with an entire lifespan. Additionally, some epigenetic molecules associated with AD etiology were also known to respond to chronic lead exposure in comparable disease models, indicating potentially interlaced mechanisms with respect to the studied neurotoxic and pathological events. Of note, epigenetic molecules acted via globally or selectively influencing the expression of disease-related genes. Compared to AD, the association of lead exposure with other neurological disorders were primarily supported by epidemiological survey, with fewer reports connecting epigenetic regulators with lead-induced pathogenesis. Some pharmaceuticals, such as HDAC (histone deacetylase) inhibitors and DNA methylation inhibitors, were developed to deal with CNS disease by targeting epigenetic components. Still, understandings are insufficient regarding the cause–consequence relations of epigenetic factors and neurological illness. Therefore, clear evidence should be provided in future investigations to address detailed roles of novel epigenetic factors in lead-induced neurological disorders, and efforts of developing specific epigenetic therapeutics should be appraised.
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Coppedè, Fabio. "Epigenetics of neuromuscular disorders." Epigenomics 12, no. 23 (December 2020): 2125–39. http://dx.doi.org/10.2217/epi-2020-0282.

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Neuromuscular disorders are a heterogeneous group of conditions affecting the neuromuscular system. The aim of this article is to review the major epigenetic findings in motor neuron diseases and major hereditary muscular dystrophies. DNA methylation changes are observed in both hereditary and sporadic forms, and combining DNA methylation analysis with mutational screening holds the potential for better diagnostic and prognostic accuracy. Novel, less toxic and more selective epigenetic drugs are designed and tested in animal and cell culture models of neuromuscular disorders, and non-coding RNAs are being investigated as either disease biomarkers or targets of therapeutic approaches to restore gene expression levels. Overall, neuromuscular disorder epigenetic biomarkers have a strong potential for clinical applications in the near future.
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Dissertations / Theses on the topic "Epigenetic disorders"

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Homs, Raubert Aïda 1983. "Epigenetic alterations in autism spectrum disorders (ASD)." Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/403885.

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The aetiology of autism spectrum disorders (ASD), a group of neurodevelopmental conditions with early onset, characterized by social and communication impairment and restricted interests, is unknown in about a third of the patients. The intense research done over the past decade has revealed a genetic contribution, while the epigenetic contribution barely begins to show. The epigenetic marks can exert an effect in gene expression without altering the underlying genetic sequence. In turn, these marks can be impaired by genetic mutations in their target sequence. Therefore, research in genomic, epigenomic and transcriptomic fields will provide convergent information to unravel the causes of ASD, necessary to establish improved diagnostic protocols and therapeutic strategies, allowing an earlier diagnosis and personalized treatment crucial for a better prognosis. Our data reveal variants associated to the phenotype which shows genetic-epigenetic interplay along with gene expression consequences. It also reveals region epigenetic variants, which follow a polygenic or complex model. Finally, we found ASD genotype-specific epigenetic marks. In the future, the progress in cost-efficiency technologies assessing epigenomics, and the availability of a reference epigenome in various tissues and cell types will provide the background to set a step-forward in establishing the developmental stage, cell types and tissues involved in the epigenetic mechanisms of the disorder.
L'etiologia dels trastorns de l'espectre autista (TEA), un grup de malalties del neurodesenvolupament d’aparició primerenca caracteritzades per problemes de comunicació, relació social, i per la presencia d’interessos restringits, és desconeguda per un terç dels individus afectats. La intensa investigació feta durant l'última dècada ha revelat una gran contribució genètica en aquesta malaltia, mentre que de l’epigenètica tot just es comença a evidenciar. Les marques epigenètiques, sense alterar la seqüència genètica subjacent, tenen un efecte en l'expressió dels gens. A la vegada, aquestes marques epigenètiques es poden veure afectades per mutacions genètiques a la seqüència. Així doncs, la recerca en genòmica, epigenòmica i transcriptòmica proporcionarà informació convergent per determinar les causes dels TEA, indispensable per establir millores en els protocols de diagnòstic i en estratègies terapèutiques, facilitant el diagnòstic precoç i el tractament personalitzat, crucial per a un millor pronòstic. Les nostres dades mostren que hi ha alteracions genètiques i epigenètiques associades al fenotip, que interactuen i tenen conseqüències sobre l’expressió gènica. També hem trobat regions amb alteracions epigenètiques, que sembla que contribueixen de manera additiva i seguint un model complex. Finalment, trobem marques epigenètiques específiques de grups de genotips TEA. En el futur, la millora de les tecnologies disponibles per avaluar l’epigenòmica, i la disponibilitat d'un epigenoma de referència en diversos teixits i tipus cel•lulars, serviran com a base per fer un pas cap endavant en l'establiment de l’etapa del desenvolupament, dels tipus cel•lulars i els teixits involucrats en els mecanismes epigenètics del trastorn.
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Modi, Bhavi P. "GENETIC AND EPIGENETIC MECHANISMS OF COMPLEX REPRODUCTIVE DISORDERS." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4574.

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Common, complex disorders are polygenic and multifactorial traits representing interactions between environmental, genetic and epigenetic risk factors. More often than not, contributions of these risk factors have been studied individually and this is especially true for complex reproductive traits where application of genomic technologies has been challenging and slow to progress. This thesis explores the potential of genetic and epigenetic components contributing to a better understanding of the biological pathways underlying disease risk in two specific female complex reproductive traits - polycystic ovary syndrome (PCOS) and preterm premature rupture of membranes (PPROM). The PCOS projects focus on characterization of a gene, DENND1A, whose association to PCOS has been established by Genome Wide Association Studies (GWAS) and is known to contribute to PCOS steroidogenic phenotype. In addition, differential microRNAs expression contributing to DENND1A expression regulation in PCOS theca cells was identified. The studies on PPROM utilize a Whole Exome Sequencing approach to identify rare variants in fetal genes contributing to extracellular matrix composition and synthesis contributing to PPROM risk. The results suggest that fetal contribution to PPROM is polygenic and is driven by a significant genetic burden of potentially damaging rare variants in genes contributing to fetal membrane strength and integrity. Tissue and location specific expression patterns of the Chromosome 21 miRNA cluster (miR-99a, miR-125b, let-7c) in fetal membranes from term pregnancies with spontaneous rupture were investigated. The results suggest that these miRNAs play potential roles in fetal membrane rupture and fetal membrane defects associated with T21.
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Kalushkova, Antonia. "Epigenetic gene regulation in multiple myeloma and mood disorders." Doctoral thesis, Uppsala universitet, Hematologi och immunologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-199494.

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Epigenetics continues to be redefined and new discoveries are likely to revolutionise the field still further. This thesis explores different aspects of how epigenetic regulation of gene expression contributes to human disease. Paper I explores the function of the IKKα kinase in regulating gene expression through the nuclear retinoic acid receptor (RAR). We define a set of genes requiring IKKα for their expression and found recruitment of IKKα to the RAR dependent on structural motifs in its protein sequence. This interplay between the NFκB pathway and nuclear receptor regulated transcription is important to consider when designing therapeutic strategies. Papers II and III focus on the plasma cell malignancy multiple myeloma (MM) and define a gene regulatory circuit defining an underexpressed gene profile in MM dependent on the Polycomb proteins. We provide proof-of-principle that the use of small chemical inhibitors may be operational in reactivating genes silenced by H3K27me3 and that this leads to decreased tumour load and increased survival in the 5T33 in vivo model of MM. We explored the genome-wide distribution of H3K27me3 and H3K4me3, and defined their association with gene expression in freshly-isolated malignant plasma cells from MM patients. Importantly, H3K27me3-marked genes in MM associated with more aggressive stages of the disease and less favourable survival. We present evidence that gene targeting by H3K27me3 is likely to not only involve a small population of tumour cells, but rather represent a common MM profile and further provide a rationale for evaluating epigenetic therapeutics in MM. Paper IV shows that pro-inflammatory gene expression in monocytes of psychiatric patients can be induced in vitro by sodium pump inhibitors, as the steroid hormone ouabain. We suggest that the ouabain-induced gene expression is regulated by an intricate network involving microRNAs, Polycomb and the H3K27me3 demethylase JMJD3. Our data indicates that epigenetic regulators play a role in transmitting cues between intrinsic and/extrinsic stimuli and gene expression in psychiatric illness. This thesis provides novel insights on how seemingly unrelated pathways may converge on transcriptional regulation and evidence that epigenetic modifiers contribute to the pathogenesis of human complex diseases such as multiple myeloma and mood disorders.
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Basil, Paul. "Epigenetic modifications associated with prenatal environmental risk factors for neurodevelopmental psychiatric disorders." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208545.

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Chan, Robin F. "Epigenetic editing to validate findings from methylome-wide association studies of neuropsychiatric disorders." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/5003.

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DNA methylation is necessary for learning, memory consolidation and has been implicated in a number of neuropsychiatric disorders. Obtaining high quality and comprehensive data for the three common forms of methylation in brain is challenging for methylome-wide association studies (MWAS). To address this we optimized a panel of enrichment methods for screening the brain methylome. Results show that these enrichment techniques approach the coverage and fidelity of the current gold standard bisulfite based techniques. Our MBD-based method can also be used with low amounts of genomic material from limited human biomaterials. Psychiatric disorders have high prevalence and are often chronic making them a leading contributor to disability. Major depressive disorder (MDD) has a lifetime prevalence of ~15% and high recurrence leading to substantial morbidity and costs to society. The underlying biological processes that contribute to MDD are poorly understood. Noting the importance of DNA methylation in neurobiology, we conducted the largest MWAS in human post-mortem brain uncover novel candidate genes and biomarkers associated with MDD. The top result of this MDD MWAS was within the gene ANKS1B. This gene has been implicated in many past genetic studies of psychiatric disorders and has experimental support as a regulator of neurotransmission. Targeted epigenetic editing technologies allow for precise modification of DNA methylation in living cells. However, an appropriate model system is critical to properly interpreting such experiments. An accelerated protocol for differentiating Ntera2 cells into human neurons was developed for this purpose. Ntera2-derived neurons express key neuronal markers and are well suited to use in epigenetic editing experiments. Concurrently, the generation of the reagents necessary for recapitulating the aberrant methylation at ANKS1B linked to MDD was undertaken. Using a modified CRISPR/Cas9 approach demethylating enzyme was directed to target sites to attempt perform editing of DNA methylation. Results indicate that significant but biologically irrelevant changes to methylation at ANSK1B were achieved. The novelty of the technology employed presented challenges to the success of the current work. However, the field of epigenetic editing is advancing rapidly and will remain an attractive method for functional characterization of future MWAS findings and basic neuroscience research.
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Ziegler, Christiane Verfasser], and Katharina [Gutachter] [Domschke. "Epigenetic Mechanisms in the Pathogenesis and Therapy of Anxiety Disorders / Christiane Ziegler ; Gutachter: Katharina Domschke." Würzburg : Universität Würzburg, 2017. http://d-nb.info/1130587916/34.

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Wells, Layne. "Investigating Neurogenesis as a Veritable Epigenetic Endophenotype for Alzheimer's Disease." Scholarship @ Claremont, 2019. https://scholarship.claremont.edu/scripps_theses/1232.

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Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by progressive amyloid plaque aggregation, neurofibrillary tangles, and cortical tissue death. As the prevalence of AD is projected to climb in coming years, there is a vested interest in identifying endophenotypes by which to improve diagnostics and direct clinical interventions. The risk for complex disorders, such as AD, is influenced by multiple genetic, environmental, and lifestyle factors. Significant strides have been made in identifying genetic variants linked to AD through the genome-wide association study (GWAS). It has been estimated in more recent years, however, that GWAS-identified variants account for limited AD heritability, suggesting the role of non-sequence genetic mechanisms, such as epigenetic moderators. By influencing gene expression, epigenetic markers have been linked to age- associated decline through modulation of chromatin architecture and global genome instability, though such mechanisms are also involved with a number of normal biological processes, including neurogenesis. As the strategies of clinical genetics shift to include a heavier focus on epigenetic contributors, altered adult neurogenesis presents itself as a strong candidate for an endophenotype of AD development. This thesis proposes that, due to neuropathological dysfunction of epigenetic mechanisms in AD, new generations of neurons fail to proliferate, differentiate, and mature correctly, resulting in the larger loss of neurons and cognitive deficits characteristic to neurodegenerative disease. The plasticity of the epigenome and the role of epigenetic factors as mediators of the genome and the environment make such alterations attractive in AD research and implies the potential for therapeutic interventions. The present review submits neurogenesis as a viable target of epigenetic research in AD, highlights shared loci between neurogenesis and AD in the epigenome, and considers the promises and limitations of the neurogenic endophenotype.
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Huang, Hsien-Sung. "Epigenetic Determinants of Altered Gene Expression in Schizophrenia: a Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/365.

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Schizophrenia is a neurodevelopmental disorder affecting 1% of the general population. Dysfunction of the prefrontal cortex (PFC) is associated with the etiology of schizophrenia. Moreover, a substantial deficit of GAD1mRNA in schizophrenic PFC has been reported by different groups. However, the underlying molecular mechanisms are still unclear. Interestingly, epigenetic factors such as histone modifications and DNA methylation could be involved in the pathogenesis of schizophrenia during the maturation of the PFC. In my work, I identified potential epigenetic changes in schizophrenic PFC and developmental changes of epigenetic marks in normal human PFC. Furthermore, mouse and neuronal precursor cell models were used to confirm and investigate the molecular mechanisms of the epigenetic changes in human PFC. My initial work examined whether chromatin immunoprecipitation can be applied to human postmortem brain. I used micrococcal nuclease (MNase)-digested chromatin instead of cross-linked and sonicated chromatin for further immunoprecipitation with specific anti-methyl histone antibodies. Surprisingly, the integrity of mono-nucleosomes was still maintained at least 30 hrs after death. Moreover, differences of histone methylation at different genomic loci were detectable and were preserved within a wide range of autolysis times and tissue pH values. Interestingly, MNase-treated chromatin is more efficient for subsequent immunoprecipitation than crosslinked and sonicated chromatin. During the second part of my dissertation work, I profiled histone methylation at GABAergic gene loci during human prefrontal development. Moreover, a microarray analysis was used to screen which histone methyltransferase (HMT) could be involved in histone methylation during human prefrontal development. Mixed-lineage leukemia 1 (MLL1), an HMT for methylation at histone H3 lysine 4 (H3K4), appears to be the best candidate after interpreting microarray results. Indeed, decreased methylation of histone H3 lysine 4 at a subset of GABAergic gene loci occurred in Mll1 mutant mice. Interestingly, clozapine, but not haloperidol, increased levels of trimethyl H3K4 (H3K4me3) and Mll1 occupancy at the GAD1 promoter. I profiled histone methylation and gene expression for GAD1 in schizophrenics and their matched controls. Interestingly, there are deficits of GAD1 mRNA levels and GAD1 H3K4me3 in female schizophrenics. Furthermore, I was also interested in whether the changes of GAD1 chromatin structure could contribute to cortical pathology in schizophrenics with GAD1 SNPs. Remarkably, homozygous risk alleles for schizophrenia at the 5’ end of the GAD1 gene are associated with a deficit of GAD1 mRNA levels together with decreased GAD1 H3K4me3 and increased GAD1H3K27me3 in schizophrenics. Finally, I shifted focus on whether DNA methylation at the GAD1 promoter could contribute to a deficit of GAD1 mRNA in schizophrenia. However, no reproducible techniques are available for extracting genomic DNA specifically from GABAergic neurons in human brain. Therefore, I used an alternative approach that is based on immunoprecipitation of mononucleosomes with anti-methyl-histone antibodies differentiating between sites of active and silenced gene expression. The methylation frequencies of CpG dinucleotides at the GAD1 proximal promoter and intron 2 were determined from two chromatin fractions (H3K4me3 and H3K27me3) separately. Consistently, the proximal promoter region of GAD1 is more resistant to methylation in comparison to intron 2 of GAD1 in either open or repressive chromatin fractions. Interestingly, overall higher levels of DNA methylation were seen in repressive chromatin than in open chromatin. Surprisingly, schizophrenic subjects showed a significant decrease of DNA methylation at the GAD1proximal promoter from repressive chromatin. Taken together, my work has advanced our knowledge of epigenetic mechanisms in human prefrontal development and the potential link to the etiology of schizophrenia. It could eventually provide a new approach for the treatment of schizophrenia, especially in the regulation of methylation at histone H3 lysine 4.
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Nawathe, Aamod. "Fetal epigenetic programming of the IGF axis in pregnancies affected by growth disorders, gestational diabetes and obesity." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/44494.

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Gestational diabetes and maternal obesity are associated with impaired maternal glycaemic control and increased risk of delivering a macrosomic fetus. Macrosomic as well as growth restricted neonates have an increased risk of metabolic syndrome and cardiovascular disease in adult life which may be mediated through an altered intra-uterine environment. The placenta acts as a mediator between the mother and the fetus and handles placental nutrient exchange and transfer. Insulin-like growth factors 1 and 2 (IGF1 and IGF2) are hormones similar to insulin and are known for their growth promoting function in the body. They are also present in the placenta and play an important role in regulating placental and fetal growth. Animal and human studies have shown that IGF1 and IGF2 deletions are associated with growth restriction. The IGFs are bound to their binding proteins called insulin-like growth factor binding proteins (IGFBPs) which modulate their bioavailability and can therefore modulate fetal growth. The IGFs and IGFBPs are associated with glucose regulation but their role in gestational diabetes is unclear. We hypothesized that the placental gene expression of IGF system related genes is altered in pregnancies complicated by fetal growth disorders (pregnancies with small or large fetuses) and in those women who had gestational diabetes mellitus (GDM) or increased body mass index (BMI > 30). Epigenetics is the study of changes in gene function that are mitotically and/or meiotically heritable and that do not entail a change in DNA sequence. DNA methylation is an epigenetic mechanism which involves addition of methyl group to a cytosine base in the DNA forming a methylated cytosine-phosphate-guanine (CpG) dinucleotide which is known to silence gene expression. This can potentially alter the expression of IGFs and their binding proteins. We have also hypothesized that a relationship existed between DNA methylation and gene expression of components of the IGF axis in the placenta. The placental IGF1 expression was found to be reduced in women with small for gestational age (SGA) neonates. The expression of IGFBPs was upregulated in SGA neonates and downregulated in large for gestational age (LGA) neonates. The placental IGF1 gene promoter was found to be hypermethylated while the promoters of the binding proteins were hypomethylated in the placentas of SGA neonates. The umbilical cord levels of IGF1 and the binding proteins in SGA and LGA neonates showed a similar trend to the placental gene expression changes. We have also analysed the placental gene expression and umbilical levels of imprinted gene GRB10 which has been investigated in mice studies and is known to cause growth restriction. We found increased placental expression of GRB10 and hypomethylation of its promoter in SGA neonates. The placental expression of IGF1, IGFBP1 and IGFBP2 was found to be decreased in women with GDM on diet and on metformin but not in those on insulin. The IGF1, IGFBP1 and IGFBP2 promoters were noted to be hypermethylated but only in women on diet treatment and not on metformin on insulin. The umbilical levels of IGF1 and IGFBP1 but not IGFBP2, were increased in GDM thus showing an inverse trend to the placental gene expression changes. In conclusion our results suggest that in SGA neonates, changes in CpG methylation contribute to the changes in gene expression of components of the IGF axis and GRB10 in fetal growth disorders. Differential methylation of the IGF1 gene, its binding proteins and GRB10 is likely to play a role in the pathogenesis of SGA neonates. Our results also suggest that GDM is associated with gene expression and epigenetic alterations in the IGF1, IGFBP1 and IGFBP2 genes, which could be part of the wider metabolic complexities associated with GDM.
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Maher, Michael. "An epigenetic approach to fatty acid metabolism in haematological malignancies." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673704.

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The role of fatty acids to overcome stress and contribute to disease progression is becoming increasingly evident in haematological diseases. Further, epigenetic factors play an important role in the aetiology of myelodysplastic syndromes (MDS) and the transformation to secondary acute myeloid leukaemia (sAML). To investigate this in the MDS/sAML cell line, SKK-1, we employed a shRNA knockdown screen to target 912 epigenetic regulators. We then coupled this loss-of-function approach to a fatty acid metabolism-based assay with which we were able to cell-sort the SKK-1 cells based on the fatty acid uptake. Here I describe the methodology of this epigenetics-metabolism approach and our efforts to validate candidate hits from the screen that were predicted to be modulators of fatty acid uptake. Following testing using single gene knockdowns of the top genes from the screen, we were not able to identify epigenetic regulators that significantly alter fatty acid uptake. In parallel, we characterised metabolic and genetic parameters of triple-sorted low (TS LOW) and high (TS HIGH) fatty acid uptake sub- populations. However, during the course of the study, we discovered latent contamination by another myeloid cell line, U-937, in our SKK-1 parental cells and TS LOW and TS HIGH sub-populations. Therefore, we interpreted results from the characterisation study with the knowledge that we had mixed cellular populations. I describe the steps we took to first identify the cell line and then our further characterisation of single cell clones of TS LOW and TS HIGH. Interestingly, we observed distinct cytogenetic profiles between single clones of TS LOW and TS HIGH, namely trisomy 8, which is a highly relevant chromosomal aberration in myeloid malignancies. Overall, this study provides a novel approach to investigate epigenetic and metabolic interactions in blood malignancies. We also find metabolically distinct sub-populations that differ by a disease-relevant karyotype.
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Books on the topic "Epigenetic disorders"

1

Epigenetics and human health: Linking hereditary, environmental, and nutritional aspects. Weinheim: Wiley-VCH, 2010.

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Cancer, autism, and their epigenetic roots. 2014.

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Wang, Fushun, Jason H. Huang, Fang Pan, and Yi-Yuan Tang, eds. Early Life Stress-Induced Epigenetic Changes Involved in Mental Disorders. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-153-6.

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Fitzgerald, Hiram E., and Leon I. Puttler, eds. Alcohol Use Disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676001.001.0001.

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Chapters in this volume reflect, to one degree or another, eight critical aspects of contemporary research attempting to understand the etiologic processes that heighten risk or resilience factors for substance use disorders: (1) a focus on systemic frameworks for understanding developmental process, (2) the heterogeneity of developmental pathways, (3) the role of genes and epigenetic–experience transactions, (4) risk cumulative/cascade models of the effects of exposure to adverse childhood experiences, (5) negotiating developmental transitional periods, (6) neurobiological embodiment of adverse childhood experiences, (7) links between alcohol use disorder and tobacco addictive behaviors, and (8) longitudinal studies and data analysis within and between studies.
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Mastroeni, Diego F. An Epigenetics Perspective on Diseases of the Central Nervous System. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0011.

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In the next two decades epigenetics could revolutionize understanding and treatment of diseases of the central nervous system. New research already demonstrates that manipulation of epigenetic mechanisms in vivo and in vitro can ameliorate a host of pathogenic processes associated with neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s (PD), amyotrophic lateral sclerosis (ALS), Huntington’s (HD), and multiple sclerosis (MS), among others. These advances have come relatively rapidly for a field that is still in its infancy compared to the much longer history of epigenetics in developmental biology. Epigenetic modifications are all-encompassing, from nucleotides to amino acids. They are capable of altering transcriptional to biochemical activity in a consistent manner across thousands of genes and hundreds of biologic pathways, yet they can do so differentially even in individuals or cells with identical gene codes. As such, epigenetic modifications are likely to touch on virtually all the mechanisms described in this book.
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Lucchesi, John C. Epigenetics, Nuclear Organization & Gene Function. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.001.0001.

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Epigenetics is the study of heritable changes in gene function that do not involve changes in the DNA sequence. Epigenetic changes, consisting principally of DNA methylation, histone modifications and non-coding RNAs, maintain and modulate the initial impact of regulatory factors that recognize and associate with particular genomic sequences. This book’s primary goal is to establish a framework that can be used to understand the basis of epigenetic regulation and to appreciate both its derivation from genetics and its interdependence with genetic mechanisms. A further aim is to highlight the role played by the three-dimensional organization of the genetic material itself (the complex of DNA, histones and non-histone proteins referred to as chromatin) and its distribution within a functionally compartmentalized nucleus. Dysfunctions at any level of genetic regulation have the potential to result in an increased susceptibility to disease or actually give rise to overt pathologies. As illustrated in this book, research is continuously uncovering the role of epigenetics in a variety of human disorders, providing new avenues for therapeutic interventions and advances in regenerative medicine.
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Gorman, Jack M. Life Events Shape Us. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850128.003.0003.

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Psychiatry downplayed the importance of life events in causing mental illness from the 1960s on, favoring a view that all disorders except one are the result of abnormal genes affecting chemical processes in the brain. Studying the exception, posttraumatic stress disorder (PTSD), when it was defined in 1980 helped lead to renewed recognition that early life adversity is central to all psychiatric conditions. At the same time, neuroscientists showed that early life experiences are capable of changing life-long behavior and brain function in laboratory animals. One mechanism by which this occurs is through the epigenetic regulation of gene expression. Epigenetics is the way that the expression levels of genes are controlled without changing the underlying genetic code. Epigenetics is an attractive way of understanding how individual life experiences are translated in the brain into each person’s unique set of emotions, behaviors, abilities, and risks for psychiatric abnormalities.
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Peedicayil, Jacob, Dennis R. Grayson, and Dag Yasui. Neuropsychiatric Disorders and Epigenetics. Elsevier Science & Technology Books, 2016.

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Neuropsychiatric Disorders and Epigenetics. Elsevier, 2017. http://dx.doi.org/10.1016/c2013-0-15470-0.

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Peedicayil, Jacob, Dennis R. Grayson, and Dimitri Avramopoulos. Epigenetics in Psychiatry. Elsevier Science & Technology Books, 2014.

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Book chapters on the topic "Epigenetic disorders"

1

Rutten, Bart P. F., and Jim van Os. "Epigenetic Epidemiology of Psychiatric Disorders." In Epigenetic Epidemiology, 343–76. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2495-2_18.

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Temple, I. Karen, Jill Clayton-Smith, and Deborah J. G. Mackay. "Imprinting Disorders of Early Childhood." In Epigenetic Epidemiology, 137–60. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2495-2_9.

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Charman, Tony, Susan Hepburn, Moira Lewis, Moira Lewis, Amanda Steiner, Sally J. Rogers, Annemarie Elburg, et al. "Epigenetic Mechanisms." In Encyclopedia of Autism Spectrum Disorders, 1135–40. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_1326.

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Fernandez, Thomas. "Epigenetic Mechanisms." In Encyclopedia of Autism Spectrum Disorders, 1814–18. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_1326.

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Woods, Rima, and Janine M. LaSalle. "Epigenetic Epidemiology of Autism and Other Neurodevelopmental Disorders." In Epigenetic Epidemiology, 321–42. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2495-2_17.

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Wang, Sung Eun, and Yong-Hui Jiang. "Epigenetic Epidemiology of Autism and Other Neurodevelopmental Disorders." In Epigenetic Epidemiology, 405–26. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94475-9_17.

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Stöger, Reinhard. "Epigenetic Epidemiology of Obesity, Type 2 Diabetes, and Metabolic Disorders." In Epigenetic Epidemiology, 401–21. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2495-2_20.

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Peterlin, Borut. "Epigenetic Biomarkers in Neurodegenerative Disorders." In Epigenetics and Human Health, 245–51. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527628384.ch19.

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Netchine, Irène, Sylvie Rossignol, Salah Azzi, and Yves Le Bouc. "Epigenetic Anomalies in Childhood Growth Disorders." In Recent Advances in Growth Research: Nutritional, Molecular and Endocrine Perspectives, 65–73. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000342568.

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López, Alberto J., Cody A. Siciliano, and Erin S. Calipari. "Activity-Dependent Epigenetic Remodeling in Cocaine Use Disorder." In Substance Use Disorders, 231–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/164_2019_257.

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Conference papers on the topic "Epigenetic disorders"

1

Tekutskaya, E., I. Raybova, and Lyubov Ramazanovna Gusaruk. "THE DEGREE OF OXIDATIVE DAMAGE TO DNA IN VITRO AS A MOLECULAR PREDICTOR OF DISORDERS CAUSED BY EPIGENETIC AND EXOGENOUS FACTORS." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.49.

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In this work, we studied the mechanisms of oxidative damage to DNA molecules isolated from whole blood of healthy donors and patients with epigenetic disease (epidermolysis bullosa) when exposed to an alternating magnetic field of low frequency in vitro, associated with the formation of reactive oxygen species.
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Erriu, Michela. "An Italian Pilot Study on Epigenetic Factors in Early Children’s Eating Disorders." In 12th International Conference on Education and Educational Psychology. European Publisher, 2021. http://dx.doi.org/10.15405/epiceepsy.21101.19.

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Vieira, Tállita Meciany Farias, Sheila Coelho Sores Lima, Franciane Gomes Andrade, Alython Araújo Chung-Filho, Claire Schwab, Christine Harrison, and Maria do Socorro Pombo-de-Oliveira. "Abstract A43: Genetic and epigenetic disorders in one cohort of acute lymphoblastic leukemia." In Abstracts: AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.tcm17-a43.

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Baraka, Kim, Francisco S. Melo, and Manuela Veloso. "Data-driven generation of synthetic behavioral feature vectors modeling children with autism spectrum disorders." In 2017 Joint IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL-EpiRob). IEEE, 2017. http://dx.doi.org/10.1109/devlrn.2017.8329808.

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Godderis, Lode, Ruxandra Nagy, Manosij Gosh, Radu Duca, and Minneke Viaene. "1713c Epigenetics in solvent induced neurobehavioral disorders." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.809.

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Claudino, Leonardo, Jane E. Clark, and Yiannis Aloimonos. "The SB-ST decomposition in the study of Developmental Coordination Disorder." In 2015 Joint IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL-EpiRob). IEEE, 2015. http://dx.doi.org/10.1109/devlrn.2015.7346131.

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Idei, Hayato, Shingo Murata, Yiwen Chen, Yuichi Yamashita, Jun Tani, and Tetsuya Ogata. "Reduced behavioral flexibility by aberrant sensory precision in autism spectrum disorder: A neurorobotics experiment." In 2017 Joint IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL-EpiRob). IEEE, 2017. http://dx.doi.org/10.1109/devlrn.2017.8329817.

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Ichinose, Koki, Jihoon Park, Yuji Kawai, Junichi Suzuki, Minoru Asada, and Hiroki Mori. "Local over-connectivity reduces the complexity of neural activity: Toward a constructive understanding of brain networks in patients with autism spectrum disorder." In 2017 Joint IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL-EpiRob). IEEE, 2017. http://dx.doi.org/10.1109/devlrn.2017.8329813.

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Yao, Zhixing, and Zaki A. Sherif. "Abstract 3698: The effect of epigenetic silencing and p53 mutation on DLL4 expression in human cancer stem cell disorder: The Li-Fraumeni syndrome." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3698.

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