Biological Determination of Mental Disorders: a Discussion Based on Recent Hypotheses from Neuroscience
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Hippocampal Neurophysiology During Exploratory Behaviour and Sleep in Rats Heterozygous for the Psychiatric Risk Gene Cacna1c
Hippocampal Neurophysiology During Exploratory Behaviour and Sleep in Rats Heterozygous for the Psychiatric Risk Gene Cacna1c Edward Richard Morrell A Thesis Presented for the Degree of Doctor of Philosophy December 2020 Word Count: 43,582 Abstract Genome-wide association studies reveal that calcium channel gene variants confer risk for psychiatric disorders across diagnostic categories. One consistently implicated gene is CACNA1C, a gene encoding the α1 pore-forming subunit of the L-type calcium channel. Recent rodent research highlights an important role for Cacna1c in hippocampal synaptic plasticity and related cognition, yet little is known about the effects of reduced Cacna1c gene dosage on hippocampal neurophysiology in vivo. Using tetrodes targeted to the dorsal CA1 I recorded single unit and local field potential activity in rats heterozygous for Cacna1c during free exploration and rest. Cacna1c heterozygous rats displayed enlarged place-fields and an associated reduction in place-cell spatial information content during runs on a linear track in a familiar and novel orientation, while place-cell activity during exploration of a novel open-field was intact. In addition, while 6-10Hz theta and 25-140Hz gamma rhythms were comparable in frequency and power in heterozygotes, their dependence on locomotion was compromised. Phase- amplitude coupling between theta and slow-gamma was also attenuated in Cacna1c heterozygous rats running on the track in a novel orientation. Hippocampal recordings at rest revealed intact 120-250Hz sharp-wave ripple oscillations, yet an enhanced participation of individual neurons in sharp-wave ripple events in Cacna1c heterozygotes. Despite the elevation in ripple-associated activity, coactivity between cell pairs during sharp-wave ripple events was markedly impaired. -
Summary Eating Disorders Are a Growing Concern Amongst Adolescent Populations
Doctorate in Educational and Child Psychology Chris Rogers Case Study 1: An Evidence-Based Practice Review Report Theme: School Based Interventions for Learning How effective are school-based universal preventive interventions at reducing eating disorder risk factors in adolescent males? Summary Eating disorders are a growing concern amongst adolescent populations. It has been argued that school-based universal preventive interventions are a convenient way to try and address this issue due to their wide-reaching access to adolescents in society through the education system. Interventions of this kind can be administered to whole cohorts of adolescents with the aim of ameliorating risk factors of eating disorders, preventing acquisition of eating disorders in later life. Research around eating disorders typically focuses on females due to larger numbers of diagnoses in this population, but males are becoming more of a focus due to their increasing rates of diagnoses. Research suggests though that preventive interventions for eating disorders are developed around findings focussed on females. This review analysed studies to assess how effective these kinds of interventions are with male adolescents. After in depth analysis of five studies, it was found that these interventions have little impact on reducing risk factors for eating disorders with male adolescents. Issues regarding the measures used by the studies and bias towards the needs of females were discussed, as well as areas for future development. 1 Doctorate in Educational and Child Psychology Chris Rogers Introduction The prevalence of eating disorders in adolescent populations has been of significance for many years and is still an ongoing area of research (Maganto, Garaigordobil, & Kortabarria, 2016; Muise, Stein, & Arbess, 2003; Neumark-Sztainer, 1996; Shisslak, Crago, Neal, & Swain, 1987). -
Biological Psychiatry Sketched—Past, Present, and Future
1 BIOLOGICAL PSYCHIATRY SKETCHED—PAST, PRESENT, AND FUTURE Jaak Panksepp J.P. Scott Center for Neuroscience Mind & Behavior, Department of Psychology, Bowling Green State University, Bowling Green, Ohio OVERTURE It is a difficult task to capture the history of biological psychiatry in a brief essay. Let me frame this modest effort in a timeless humanistic perspective. Psychiatry is the study and treatment of troubled mental lives. Its ultimate goal is to heal broken spirits. At its core, it is an attempt to better understand human thoughts and emotions and to allow this understanding to inform the healing arts. Despite our modern scientific hubris, we know rather little about how brains truly construct our minds and passions. Partly, this is because few scholars have come to terms with the need to understand the evolutionary neural dynamics that affective experiences are ultimately made of. It is all too easy to accept emotions as primitive “givens” and proceed toward a superficial understanding based on words, arbitrary definitions, and the quiddities of logic rather than biology. But the greater and more significant Textbook of Biological Psychiatry, Edited by Jaak Panksepp ISBN 0-471-43478-7 Copyright 2004 John Wiley & Sons, Inc. 3 4 BIOLOGICAL PSYCHIATRY SKETCHED—PAST, PRESENT, AND FUTURE depths of this mystery have to be plumbed by an integrative neuroscience that has barely emerged. It is surely not off the mark to claim that the single most important scientific question for biological psychiatry is the accurate decoding of the basic neural nature of affective values and related cognitive experiences. Emotions and moods guide most of our thinking processes and behavioral choices, whether well-arranged or deranged. -
Review Synaptic Functions and Their Disruption in Schizophrenia: from Clinical Evidence to Synaptic Optogenetics in an Animal Model
No. 5] Proc. Jpn. Acad., Ser. B 95 (2019) 179 Review Synaptic functions and their disruption in schizophrenia: From clinical evidence to synaptic optogenetics in an animal model † By Kisho OBI-NAGATA,*1 Yusuke TEMMA*1 and Akiko HAYASHI-TAKAGI*1,*2, (Communicated by Nobutaka HIROKAWA, M.J.A.) Abstract: The adult human brain consists of approximately a hundred billion neurons, which are connected via synapses. The pattern and strength of the synaptic connections are constantly changing (synaptic plasticity), and these changes are considered to underlie learning, memory, and personality. Many psychiatric disorders have been related to disturbances in synaptogenesis and subsequent plasticity. In this review, we summarize findings of synaptic disturbance and its involvement in the pathogenesis and/or pathophysiology of psychiatric disorders. We will focus on schizophrenia, because this condition has a high proven heritability, which offers more unambiguous insights into the biological origins of not only schizophrenia but also related psychiatric disorders. To demonstrate the involvement of synaptopathy in psychiatric disorders, we discuss what knowledge is missing at the circuits level, and what new technologies are needed to achieve a comprehensive understanding of synaptopathy in psychiatric disorders. Keywords: synaptopathy, schizophrenia, synaptic integration, optogenetics, AS-PaRac1 tally alter neural outcomes. Epidemiological, devel- Introduction opmental and neuroimaging studies have indicated Human brain development is a protracted that -
American Psychiatric Association 1999 Annualmeeting
1999 SCIENTIFIC PROGRAM COMMITTEE Seated (left to right): Drs. Ordonca. Levin, Ruiz, Butterfield. Balon, Shaffi. 1st Row Standing (left to right): Drs. Belfer. Pena. Vergare, Pi. Spitz. Mega. McDowell. Goldfinger, Val, Lu, Tamminga. 2nd Row Standing (left to right): Drs. Ratner. Hamilton. Weissman. Ramox, Cutler. Dudley. Millman. Book. May 15,1999 Dear Colleagues and Guests: Welcome to the 152nd Annual Meeting of the American Psychiatric Association. This is the occasion when organized psychiatry displays its might in one of the largest educational, social and political medical gatherings in the world. The theme for 1999 is easy to remember, "The Clinician" I chose this theme because it represents the professional lives of most psychiatrists. I want to pay tribute to the attitudes, the skills and the knowledge of those who see patients day in and day out Research has given precision to our diagnoses and effectiveness to our treatments We are winning the war against anxiety and mood disorders, the psychoses, chemical dependence and the disorders resulting from structural damage to the brain. Psychotherapy and psychotropics are increasingly better targeted. We are going to dialogue about new initiatives in mental health financing. Radical reform is possible with the use of tax exemptions-vouchers, defined contributions (as opposed to the fine benefits), and consolidation of programs to enhance individual control. Our presentations here are going to show that the business community can join us in the protection of the working community. Employees are not costs but assets, the human capital is the best source of profits, and the employers should work better with physicians and not with insurance companies. -
[For Consideration As Part of the ENIGMA Special Issue] Ten Years
[For consideration as part of the ENIGMA Special Issue] Ten years of Enhancing Neuro-Imaging Genetics through Meta-Analysis: An overview from the ENIGMA Genetics Working Group Sarah E. Medland1,2,3, Katrina L. Grasby1, Neda Jahanshad4, Jodie N. Painter1, Lucía Colodro- Conde1,2,5,6, Janita Bralten7,8, Derrek P. Hibar4,9, Penelope A. Lind1,5,3, Fabrizio Pizzagalli4, Sophia I. Thomopoulos4, Jason L. Stein10, Barbara Franke7,8, Nicholas G. Martin11, Paul M. Thompson4 on behalf of the ENIGMA Genetics Working Group 1 Psychiatric Genetics, QIMR Berghofer Medical Research Institute, Brisbane, Australia. 2 School of Psychology, University of Queensland, Brisbane, Australia. 3 Faculty of Medicine, University of Queensland, Brisbane, Australia. 4 Imaging Genetics Center, Mark and Mary Stevens Neuroimaging and Informatics Institute, Keck School of Medicine of USC, University of Southern California, Marina del Rey, CA, USA. 5 School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia. 6 Faculty of Psychology, University of Murcia, Murcia, Spain. 7 Department of Human Genetics, Radboud university medical center, Nijmegen, The Netherlands. 8 Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, The Netherlands. 9 Personalized Healthcare, Genentech, Inc., South San Francisco, USA. 10 Department of Genetics & UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, USA. 11 Genetic Epidemiology, QIMR Berghofer Medical Research Institute, Brisbane, Australia. Abstract Here we review the motivation for creating the ENIGMA (Enhancing NeuroImaging Genetics through Meta Analysis) Consortium and the genetic analyses undertaken by the consortium so far. We discuss the methodological challenges, findings and future directions of the Genetics Working Group. -
2017 Annual Meeting Guide
#APAAM17 psychiatry.org/ annualmeeting to the 2017 Annual Meeting Prevention Through Partnerships About This Guide psychiatry.org/annualmeeting In this book, you will find three sections: Program, New Research and the Exhibits Guide. Use these sections to navigate the 2017 Annual Meeting and experience all the meeting has to offer. Located within the Program, you will find a description of the various scientific session formats along with a log where you can record your daily attendance for the purpose of obtaining CME credit for your activities. The Program is first organized by day, then by session start time, with formats and sessions listed alphabetically under those times. Individual meeting days and program tracks are color- coded to make navigating the Program simple and easy. The New Research section lists the posters that will be presented at this meeting, organized numerically by session/day. There is a topic index at the end of the New Research section to assist you in finding the posters most interesting to you. The Exhibits Guide contains an acknowledgement to exhibitors for sponsorships, a list of the exhibitors and a floor plan of the Exhibit Hall, along with information about the Product Theaters, Therapeutic Updates, Career Fair, and Publishers Book Fair. Use this guide and the included exhibitor and author/presenter indices to navigate the exhibit hall and find precisely the booth you’re looking for. If you have any questions about this book or the scientific program, please feel free to stop by the Education Center, Ballroom 20 Foyer, Upper Level, San Diego Convention Center, and a member of the APA Administration will be happy to assist you. -
Genetics Contributes to Mental Health Risks in Adoptees
Media contact Rhiannon Bugno +1 214 648 0880 [email protected] Genetics contributes to mental health risks in adoptees Genetics and early life stress both important factors for mental health problems in adults adopted as children, says large genetic risk study in Biological Psychiatry Philadelphia, January 29, 2020 – The adoption of children is a fundamental method of building families. However, adoptees may face subsequent adaptive challenges associated with family stress at the time of birth and during the adoption process. It should be no surprise, then, that adoptees have a small but well-known increased risk for depression, anxiety and other mental health disorders. The health effect has been attributed to stressful early childhoods. But genetics also plays a role, according to a large new study published in Biological Psychiatry, published by Elsevier. “We found adopted individuals on average had a somewhat higher genetic risk for mental health problems, but the effects are quite small,” said lead author Kelli Lehto, PhD, a postdoctoral researcher at Karolinska Institute in Stockholm. “Overall, the main message here is that both environment and genetics are important.” Psychiatric disorders, including depression, anxiety and schizophrenia are, to varying degrees, heritable. Genome-wide association studies (GWAS) have identified a growing number of genetic markers associated with the risk for most major psychiatric disorders so that a ‘polygenic risk score’ for these disorders may be estimated. Dr. Lehto and colleagues analyzed the genomic and health information data of 243,797 participants in the UK Biobank, a major health resource established by the Wellcome Trust and others, including a group of 3,151 who were adopted as children within Britain, mostly in the 1950s and 1960s. -
Psychiatric Genetics and the Structure of Psychopathology
Molecular Psychiatry https://doi.org/10.1038/s41380-017-0010-4 EXPERT REVIEW Psychiatric genetics and the structure of psychopathology 1,2,3 4,5 6 7 7 Jordan W. Smoller ● Ole A. Andreassen ● Howard J. Edenberg ● Stephen V. Faraone ● Stephen J. Glatt ● Kenneth S. Kendler8,9 Received: 20 July 2017 / Revised: 23 October 2017 / Accepted: 1 November 2017 © Macmillan Publishers Limited, part of Springer Nature 2017 Abstract For over a century, psychiatric disorders have been defined by expert opinion and clinical observation. The modern DSM has relied on a consensus of experts to define categorical syndromes based on clusters of symptoms and signs, and, to some extent, external validators, such as longitudinal course and response to treatment. In the absence of an established etiology, psychiatry has struggled to validate these descriptive syndromes, and to define the boundaries between disorders and between normal and pathologic variation. Recent advances in genomic research, coupled with large-scale collaborative efforts like the Psychiatric Genomics Consortium, have identified hundreds of common and rare genetic variations that contribute to a range of neuropsychiatric disorders. At the same time, they have begun to address deeper questions about the structure and classification of mental disorders: To what extent do genetic findings support or challenge our clinical 1234567890 nosology? Are there genetic boundaries between psychiatric and neurologic illness? Do the data support a boundary between disorder and normal variation? Is it possible to envision a nosology based on genetically informed disease mechanisms? This review provides an overview of conceptual issues and genetic findings that bear on the relationships among and boundaries between psychiatric disorders and other conditions. -
Social–Emotional Functioning in Young People with Symptoms of Eating Disorders: a Gender Inclusive Analogue Study
Received: 18 November 2019 | Revised: 14 October 2020 | Accepted: 12 December 2020 DOI: 10.1002/brb3.2017 ORIGINAL RESEARCH Social–emotional functioning in young people with symptoms of eating disorders: A gender inclusive analogue study Ashley Boscoe | Rebecca Stanbury | Amy Harrison Department of Psychology and Human Development, Institute of Education, Abstract University College London, London, UK Introduction: Contemporary models of eating disorders (EDs) suggest that EDs are Correspondence maintained by social–emotional difficulties. However, supporting evidence is derived Amy Harrison, Department of Psychology largely from female, clinic-based samples. This study, which refrained from gender and Human Development, Institute of Education, University College London, 25 specific inclusion criteria, aimed to improve understanding of social–emotional func- Woburn Square, London WC1H 0AA, UK. tioning in a large community-based analogue sample of young adults aged 16–26. Email: [email protected] Methods: Five hundred and forty-four participants (85.1% female; mean age Funding information 21, SD 4.3) completed the Eating Attitudes Test, Clinical Outcomes in Routine Dr Amy Harrison acknowledges support = from The Medical Research Council, Grant Evaluation, Difficulties in Emotion Regulation Scale, Social Phobia Inventory, Revised reference: S0197071/1. Social Anhedonia Scale, Toronto Alexithymia Scale, and the Reading the Mind in the Eyes Task. Results: One hundred and sixty-four participants scored over the EAT-26 clinical cutoff, and a two-way multivariate analysis of covariance found a medium-sized, statistically significant main effect of group on social–emotional functioning (F(5, 530) = 6.204, p ≤ .001, Wilks' Λ = 0.945, d = 0.48.), suggesting that individuals with significant ED symptoms found it more challenging to notice, label, and regulate emo- tions in themselves and recognize emotions in others. -
The Neurobiology of Mood and Psychotic Disorders Jacqueline A
The Neurobiology of Mood and Psychotic Disorders Jacqueline A. Clauss, MD, PhD Clinical and Post-Doctoral Fellow, Division of Child and Adolescent Psychiatry, Department of Psychiatry, Massachusetts General Hospital Clinical Fellow, Division of Child and Adolescent Psychiatry, McLean Hospital Daphne Holt, MD, PhD Co-Director, Schizophrenia Clinical and Research Program Department of Psychiatry, Massachusetts General Hospital Associate Professor, Harvard Medical School www.mghcme.org Disclosures Neither I nor my spouse has a relevant financial relationship with a commercial interest to disclose. www.mghcme.org Disorder incidence and overlap • Major Depressive Disorder (MDD) Overall lifetime incidence: 17% in the U.S. (lower in other countries, e.g., in Japan 3%) Among those with MDD, lifetime incidence of psychosis: ~18% • Bipolar Disorder (BD) Overall lifetime incidence: ~4% (including Bipolar I & II and subthreshold); 1% for Bipolar I Among those with BD, lifetime incidence of psychosis: 25% • Schizophrenia (SZ) Overall lifetime incidence: 0.7%, ~3% defined broadly (with 5+ fold variation in incidence across the world, highlighting the importance of environmental factors) Among those with SZ, lifetime incidence of MDD: 25% • Genetics and neuroimaging studies show evidence for biological overlap and specificity (to symptoms or diagnostic category) Overlap vs. diagnostic specificity: Bipolar 1–linked genes overlap most with schizophrenia-linked genes, Bipolar II-linked genes overlap most with depression-linked genes The Bipolar Disorder -
Genetics Factors Contributing to Body Weight in Anorexia Nervosa And
Genetics Factors Contributing to Body Weight in Anorexia Nervosa and Bulimia Nervosa by Zeynep Yilmaz A thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy (PhD) Institute of Medical Science University of Toronto © Copyright by Zeynep Yilmaz (2013) Genetic Factors Contributing to Body Weight in Anorexia Nervosa and Bulimia Nervosa Zeynep Yilmaz Doctor of Philosophy (PhD) Institute of Medical Science University of Toronto 2013 Abstract Anorexia nervosa (AN) is an eating disorder (ED) with substantial morbidity and the highest mortality among psychiatric disorders. Low body mass index (BMI) is the sine qua non of AN, and behaviours associated with reaching it are the primary reason for AN’s high morbidity and mortality. Low BMI is also the main criterion diagnostically separating AN from bulimia nervosa (BN). The aim of this dissertation was to determine the role of genes regulating weight and appetite in BMI in AN and BN. Study 1 utilized carefully selected DNA samples to explore the role of markers in the leptin, melanocortin, and neurotrophin system genes with known or putative function in AN, BN, and controls, as well as in lifetime BMIs in EDs. Study 2 investigated dopamine pathway genes and FTO in weight regulation in a large sample of AN cases. The results revealed that an MC4R variant linked to antipsychotic-induced weight gain was underrepresented in AN, and AGRP and NTRK2 genetic variants were linked to minimum BMI in AN and maximum BMI in BN, respectively. In Study 2, a significant association between FTO and BMI at recruitment was observed.