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  1. Home
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  3. Principles of Psychiatric Genetics
  • Cited by 3
Publisher:
Cambridge University Press
Online publication date:
October 2012
Print publication year:
2012
Online ISBN:
9781139025997
DOI:
https://doi.org/10.1017/CBO9781139025997
Subjects:
Psychiatry and Clinical Psychology, Neurology and Clinical Neuroscience, Medicine, Psychiatry
Information

Book description

Disorders of behavior represent some of the most common and disabling diseases affecting humankind; however, despite their worldwide distribution, genetic influences on these illnesses are often overlooked by families and mental health professionals. Psychiatric genetics is a rapidly advancing field, elucidating the varied roles of specific genes and their interactions in brain development and dysregulation. Principles of Psychiatric Genetics includes 22 disorder-based chapters covering, amongst other conditions, schizophrenia, mood disorders, anxiety disorders, Alzheimer's disease, learning and developmental disorders, eating disorders and personality disorders. Supporting chapters focus on issues of genetic epidemiology, molecular and statistical methods, pharmacogenetics, epigenetics, gene expression studies, online genetic databases and ethical issues. Written by an international team of contributors, and fully updated with the latest results from genome-wide association studies, this comprehensive text is an indispensable reference for psychiatrists, neurologists, psychologists and anyone involved in psychiatric genetic studies.

Reviews

'A magnificent and timely contribution. I especially enjoyed Dan Geschwind's chapter on autism.'

Solomon Snyder - University Distinguished Service Professor of Neuroscience, Pharmacology and Psychiatry, The Johns Hopkins University School of Medicine

'It is highly suitable as a starting point for those who find themselves on the continuum between practising clinicians and specialists in biological psychiatry.'

Source: Psychological Medicine

'The contributing authors are all prominent, expert members of their fields … Principles of Psychiatric Genetics … is a demonstration of how much the field has progressed and an indication toward a promising future.'

Source: American Journal of Psychiatry

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Contents

Page 2 of 2

Contents
  • Chapter 25 - Genetics of stimulant dependence
    pp 306-315
  • View abstract

    Summary

    Genetic analyses which are relevant to plant and animal studies, rather than human populations, have specific limitations in relation to the genetics of schizophrenia. Some reviewers of family studies of schizophrenia have drawn the conclusion that schizophrenia and bipolar disorder do not share the same genetic etiologies whereas others argue that they often do. Considerable effort has been focused on genetic linkage analysis of schizophrenia employing genetic markers in multiply affected families to identify which chromosomal regions harbor susceptibility genes. This approach must take into account the complication of heterogeneity of linkage in which a number of susceptibility genes localized to different chromosomes contribute to the development of schizophrenia. The chapter describes a selection of genes that have been implicated in susceptibility to schizophrenia by cytogenetic, linkage and/or association studies. Twin and adoption studies have shown that the family environment has no influence on the etiology of schizophrenia.
  • Chapter 26 - Genetics of personality disorders
    pp 316-323
  • View abstract

    Summary

    Anorexia nervosa (AN) and bulimia nervosa (BN) are related disorders of unknown etiology that most commonly begin during adolescence in women. AN and BN individuals commonly have clusters of puzzling symptoms. Twin studies of AN and BN suggest there is approximately a 50-80% genetic contribution to liability accounted for by additive genetic factors. Psychologically, change may challenge the rigidity of those at risk for AN and BN, and thus open a window of vulnerability. The Price Foundation, a private, European-based foundation, has supported a multicenter international collaboration to investigate the genetics of AN and BN. In an exploration of how behavioral covariates enhanced the linkage signals, Devlin and colleagues evaluated features of ED for the following criteria: consistent relationship to eating pathology; heritability; and relationship to severity of some aspect of the disorder. Some studies evaluating dopaminergic and serotonergic candidate genes for association with AN are reviewed in this chapter.
  • Chapter 27 - Ethical issues in behavioral genetics
    pp 324-335
  • View abstract

    Summary

    Many studies have estimated heritability of body mass index (BMI) and related variables, and they are consistent in finding moderate to high heritability. Genes central to energy balance tend to have low variability, presumably because of strong selection pressure. Even so, some have argued that mutations in a large number of genes may account for most human obesity and other common diseases. Substantial progress in finding rare variants has come with a focus on copy number variation (CNV). Whole genome association (WGA) studies have several advantages over whole genome linkage scans. Gene-environment interaction can play an important role in the development of obesity, although it should be born in mind that this may only complicate things further, as environmental response is itself heritable. Epigenetics are discussed in this chapter. WGA studies results have demonstrated that there are indeed common variants in genes that increase risk for obesity.
  • Chapter 28 - Genetics of Tourette syndrome and related disorders
    pp 336-346
  • View abstract

    Summary

    This chapter focuses on alcohol dependence (alcoholism), because the diagnosis is more reliable and because most of the genetic data focus on dependence. The earliest genetic association studies in alcoholism were candidate gene studies targeting coding variations in the genes that metabolize alcohol. Certain variations in alcohol dehydrogenases (ADH) and aldehyde dehydrogenases (ALDH) genes have very strong effects on the risk for alcoholism. Variations in other genes appear to have a much smaller effect on risk. Linkage studies and their follow-up, along with candidate gene studies and genome-wide association studies (GWAS), are beginning to fill the gaps. Initial findings must be confirmed in independent studies, and much work remains to elucidate the mechanisms involved. The future will involve studies of epigenetic factors, copy number variants, and gene expression, as well as tests for rare variants of large effect in specific families.
  • Chapter 29 - Endophenotypes in psychiatric genetics
    pp 347-362
  • View abstract

    Summary

    Understanding the genetics of nicotine dependence can lead to targeted treatments and ultimately significantly decrease tobacco-associated morbidity and mortality. In the study of nicotine dependence, it is important to understand the behavioral progression to nicotine dependence when choosing a control group. Some researchers argue that smoking is a means of self-medicating and nicotine dependence is therefore caused by mental illness. Genome-wide association studies (GWAS) have found associations between nicotine dependence and the a5 nicotinic receptor subunit gene. This chapter postulates that there are at least two distinct biological mechanisms that alter the risk of nicotine dependence. The first biological mechanism is caused by an amino acid change in CHRNA5, in the non-synonymous SNP rs16969968. The second mechanism altering risk of nicotine dependence is through altered expression of the α5 mRNA. Associations in this region have also been found in lung disease.
  • Chapter 30 - Developmental disorders
    pp 363-370
  • View abstract

    Summary

    This chapter presents several experimental approaches performed in the Laboratory of the Biology of Addictive Diseases to characterize the relationship of gene variations with heroin addiction and pharmacogenomics. Although opioid receptors often subserve similar physiological functions, activation of the kappa-opioid receptor (KOPr) by exogenous agonists produces dysphoria in humans and aversive effects in experimental animals, in contrast to activation of mu-opioid receptor (MOPr). Opiate addiction is a chronic relapsing disorder that is treated world-wide with methadone. The genes studied are usually those which have been shown to be involved in some aspects of development of addiction. In some studies, multiple genes, all hypothesized to be potentially involved in opioid addiction, have been studied. In other cases, genome-wide association studies (GWAS) have been performed to identify regions of chromosomes which may influence vulnerability to the development of addiction. These studies usually do not identify specific genes within chromosome regions.
  • Chapter 31 - Alzheimer's disease
    pp 371-381
  • View abstract

    Summary

    This chapter reviews evidence supporting the hypothesis that genetic inheritance plays a substantial role in dependence on cocaine and (to a less well-studied degree) other illicit psychostimulants. The role of genes in cocaine dependence, however, may largely reflect a more general liability to develop dependence on a variety of substances. Studies of molecular genetic mechanisms in cocaine dependence remain in an early stage of development. A genome-wide association study (GWAS) of methamphetamine dependence, while yielding some interesting leads, requires replication in light of its small size, and reliance on pooled genotyping. While several intriguing candidate-gene associations between specific loci and cocaine dependence have been reported, to date there has yet to be a definitively replicated result reported. Clearly, more work is required in the human genetics of stimulant dependence, to identify and characterize how specific genes influence risk for this set of disorders.

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