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"Psychiatric disorders are highly prevalent and one of the leading causes of disease burden worldwide. Nevertheless, there are no validated biomarkers to be used for either diagnostic or prognostic purposes and their etiology remains largely unknown. Thanks to heritability studies, it has been recognized that both nature (genetics) and nurture (environment) contribute to the onset of mental disorders. Accordingly, exposure to both prenatal stress and childhood maltreatment has been reliably identified as a risk factor for a wide range of psychiatric disorders. However, not all individuals facing this kind of early environmental insults ends up developing psychopathological conditions. Thus, gene—environment (GxE) interactions have been proposed to be involved in the physiopathology of mental disorders; epigenetic mechanisms such as DNA methylation have been hypothesized to mediate these interactions. In this framework, the present dissertation aimed to disentangle the role of DNA methylation both in increasing anxious-depressive liability, and embedding the experience of severe prenatal stress, thanks to two independent samples of monozygotic twins. NR3C1 gene, encoding the glucocorticoid receptor, was selected as a candidate gene of interest due to its crucial role in the regulation of the stress response. A systematic review of the available scientific literature revealed a great interest in NR3C1 methylation, and specifically in its exon 1F, in the context of both exposure to stress and stress-related disorders, highlighting the association between exposure to early life stress and NR3C1 hypermethylation. Additionally, this revision also pointed out the lack of studies regarding other promoter regions of this gene. Thus, we explored NR3C1 exon 1D methylation near a glucocorticoid responsive element (GRE) describing its association with both (i) the familial component of anxious-depressive liability, and (ii) hippocampal connectivity within the brain emotional network. Our second candidate gene of interest was SLC6A4, encoding the serotonin transporter, which is the primary pharmacological target of the most widely prescribed antidepressants to date (SSRIs). Again, a systematic review of the literature revealed the association between SLC6A4 methylation and exposure to early life stress, further suggesting its mediator role in previously discussed GxE interactions involving a long polymorphic region of this gene (5-HTTLPR). Complementarily, we assessed SLC6A4 methylation in a CpG island shore region characterized by a sex-differential methylation pattern; specifically, women exhibit higher methylation at this region when compared to men. Remarkably, we found an association between methylation at this region and the presence of somatization symptoms, suggesting the involvement of SLC6A4 methylation in known sexual differences regarding internalizing psychopathology globally. Since epigenetic signatures can arise in a stochastic fashion, monozygotic twins were also analyzed to identify methylation outliers which could potentially contribute to anxious-depressive psychopathology. In this regard, we reported the presence of methylation outliers in genes previously involved in neuropsychiatric disorders. Finally, the role of prenatal stress in fetal DNA methylation signatures was also explored. First, a meta-analysis on maternal psychosocial stress experienced during pregnancy and newborn NR3C1 methylation exhibited the association between both variables in line with non-genetic intergenerational transmission of stress hypotheses. On the other hand, a sample of monochorionic monozygotic newborn twins exposed to several prenatal complications was epigenomically assessed with regard to an obstetric routine measure predictive of perinatal morbid risk. The latter study revealed newborns exposed to prenatal stress during the third trimester of pregnancy exhibit developmental immaturity in terms of epigenetic (DNA methylation based) age; furthermore, differential CpG-specific methylation was found in EP300 gene, a previously identified candidate gene conferring risk for schizophrenia and involved in hypoxia response. Together, these findings support the notion that DNA methylation is involved both in the embedding of early life stress exposure and the pathophysiology of several psychiatric disorders." -- TDX.
Designed to accompany the SCID-D, this guide instructs the clinician in the administration, scoring and interpretation of SCID-D interview. The Guide describes the phenomenology of dissociative symptoms and disorders, as well as the process of differential diagnosis. This revised edition includes a set of decision trees and four case studies.
This state-of-the-art work has been highly praised for bridging the divide between adult and developmental psychopathology. The volume illuminates the interplay of biological, cognitive, affective, and social-environmental factors that place individuals at risk for psychological disturbance throughout development. Childhood-onset and adult forms of major disorders are examined in paired chapters by prominent clinical researchers. An integrative third chapter on each disorder then summarizes what is known about continuity and change in vulnerability across the lifespan. Implications for assessment, treatment, and prevention are also considered.
Perinatal psychiatry is an emerging field that investigates the role of perinatal events – for example pregnancy complications and infections – in the development of neuropsychiatric conditions, such as schizophrenia and mood disorders. Among the implicated pathological mechanisms, perinatal-induced inflammation seems to play a major role and is being considered as a potential target for therapeutic intervention. Bringing together various approaches in the field (preclinical and clinical, epidemiological, immunological and genetic methods), the book discusses the available evidence, the putative mechanisms and the challenges ahead.
"In Scared Sick, childhood expert and therapist Robin Karr-Morse and lawyer and strategist Meredith Wiley propose that chronic fear experienced in infancy and early childhood lies at the root of numerous diseases as well as emotional and behavioral pathologies in adults."--Jacket.
Age at onset studies have been an important approach to understanding disease across all medical specialties. Over the last few decades, genetic research has led to the identification of unique genes and, in some cases, physiologically different disorders. These advances bring us closer to identifying genetic vulnerability and implementing prevention programs for psychopathology. Childhood Onset of "Adult" Psychopathology: Clinical and Research Advances provides an understanding of the childhood onsets of adult psychiatric disorders, including when and in what sequence psychiatric disorders begin in childhood, and how these disorders evolve over the life span. This book examines Studies on the growing volume of data on very early forms of depression, criminality, alcoholism, schizophrenia, and anxiety Genetics, evolution, and the significance of age at onset in terms of individual variability and the course of disease The biological manner in which early-onset disorders progress New insights into the disease etiology of schizophrenia and the neurodevelopmental hypothesis The long-debated subject of whether depressive disorder in preadolescent children is the same as depressive disorder in adults and studies of individuals at risk for disorders of anxiety and depression The implications for prevention of adult psychiatric disorders, alcoholism, and antisocial personality disorder Complete with extensive references and tables, this text provides practitioners with a better understanding of adult psychopathology and insight into early detection and prevention methods.
This handbook is currently in development, with individual articles publishing online in advance of print publication. At this time, we cannot add information about unpublished articles in this handbook, however the table of contents will continue to grow as additional articles pass through the review process and are added to the site. Please note that the online publication date for this handbook is the date that the first article in the title was published online.
There is now ample evidence from the preclinical and clinical fields that early life trauma has both dramatic and long-lasting effects on neurobiological systems and functions that are involved in different forms of psychopathology as well as on health in general. To date, a comprehensive review of the recent research on the effects of early and later life trauma is lacking. This book fills an obvious gap in academic and clinical literature by providing reviews which summarize and synthesize these findings. Topics considered and discussed include the possible biological and neuropsychological effects of trauma at different epochs and their effect on health. This book will be essential reading for psychiatrists, clinical psychologists, mental health professionals, social workers, pediatricians and specialists in child development.
"..a blending of two important approaches to understanding psychopathology- the developmental approach and the vulnerability approach. I think a book like this is timely, is needed, and would be of interest to professors who teach courses in psychopathology at the advanced undergraduate and graduate levels." — Robin Lewis, Old Dominion University "Bringing together developmental psychopathology frameworks and the vulnerability-stress models of psychological disorders is an excellent idea. I am aware of no other book that incorporates these two approaches. Having taught Psychopathology courses for both master′s and doctoral students, I reviewed many books to recommend and use in the courses. It is my belief that a book of this type is needed particularly for graduate students." —Linda Guthrie, Tennessee State University Edited by Benjamin L. Hankin and John R. Z. Abela, Development of Psychopathology: A Vulnerability-Stress Perspective brings together the foremost experts conducting groundbreaking research into the major factors shaping psychopathological disorders across the lifespan in order to review and integrate the theoretical and empirical literature in this field. The volume editors build upon two important and established research and clinical traditions: developmental psychopathology frameworks and vulnerability-stress models of psychological disorders. In the past two decades, each of these separate approaches has blossomed. However, despite the scientific progress each has achieved individually, no forum previously brought these traditions together in the unified way accomplished in this book. Key Features: Consists of three-part text that systematically integrates vulnerability-stress models of psychopathology with a developmental psychopathological approach. Brings together leading experts in the field of vulnerability, stress, specific vulnerabilities to psychological disorders, psychopathological disorders, and clinical interventions. Takes a cross-theoretical, integrative approach presenting cutting-edge theory and research at a sophisticated level. Development of Psychopathology will be a valuable resource for upper-division undergraduate and graduate students in clinical psychology, as well as for researchers, doctoral students, clinicians, and instructors in the areas of developmental psychopathology, clinical psychology, experimental psychopathology, psychiatry, counseling psychology, and school psychology.