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PubMed1996

Ernst Rüdin (1874-1952) and his genealogic-demographic department in Munich (1917-1986): an introduction to their family studies of schizophrenia.

This historical review introduces a series of papers abstracting, reanalyzing and commenting upon family studies of schizophrenia conducted by Ernst Rüdin and his geneologic-demographic department in Munich. These studies, which pioneered many of the methods still critical to psychiatric genetics, are little known in the anglophonic world. Starting with a study of schizophrenia in siblings, members of the Rüdin school expanded to study a wide range of relationships (including grandchildren and nieces/nephews) and disorders (including affective illness, obsessive-compulsive disorder, epilepsy and personality disorders). They examined many methodologic issues in psychiatric genetics including i) ascertainment correction, ii) anticipation, iii) age correction, iv) assortative mating, v) reduced fertility, vi) spectrum disorders, and vii) familial transmission of age at onset. After the rise of Hitler in Germany, Rüdin and his institute became involved in the eugenic policies of the Nazis, raising important questions about possible political abuse of scientific findings in general and those from the field of psychiatric genetics in particular.

Demography↗
PubMed2005

Genetics of developmental psychiatric disorders: pathways to discovery.

Genetics has captured the imagination of the public, the interest of the media and a large place in the sciences. Since the discovery of the structure of DNA by Watson and Crick, the double helix has epitomized the main dogma of genetics: everything from the tiniest details of the human body to the most complex of behaviours is encoded in the genes. This belief has been strengthened by the tremendous success that has been achieved in cloning more than 1000 genes that cause simple Mendelian disorders. However, for complex disorders, particularly psychiatric conditions, the search for genes has been frustrating and has not yielded definitive results, although claims of gene discoveries are made regularly. In this article, we discuss the possible causes for these difficulties, along with some directions that may help in reducing these problems. We also consider the implications of psychiatric genetic research for individual and public health.

Child↗
PubMed1990

Recent advances in the genetics of psychiatric disorder.

The prediction of risk for mental illnesses that have a strong genetic basis has usually been carried out by employing empirically derived estimates of recurrence observed in family studies. Because systematic methods of mapping the human genome with DNA polymorphisms have been developed it is possible that prenatal prediction of certain mental illnesses may eventually become a more accurate method of risk prediction than the empirical method currently used. Recombinant DNA technology as used in genetic linkage studies can also specify a mode of genetic transmission and lead on to aetiological studies of the disorder. The latter will result from the molecular cloning and sequencing of the responsible genetic mutations. The use of recombinant DNA technology has enabled single-gene effects to be found in schizophrenia, manic depression and Alzheimer's disease. In highly selected families it is now possible to calculate the risk of developing certain mental illnesses by DNA testing before birth. Failure to find linkages in separate schizophrenia, manic depression and Alzheimer's disease family samples has also been reported, indicating that there is heterogeneity of linkage with genes at several distinct genetic loci that contribute susceptibility to very similar clinical disorders. Resolution of the degree to which there is heterogeneity of linkage and a further examination of the factors which influence the variable effects of the abnormal genes predisposing to mental illness will both be necessary before accurate risk prediction can become feasible.

Alzheimer Disease↗
PubMed1999

Genetics and child psychiatry: I Advances in quantitative and molecular genetics.

Advances in quantitative psychiatric genetics as a whole are reviewed with respect to conceptual and methodological issues in relation to statistical model fitting, new genetic designs, twin and adoptee studies, definition of the phenotype, pervasiveness of genetic influences, pervasiveness of environmental influences, shared and nonshared environmental effects, and nature-nurture interplay. Advances in molecular genetics are discussed in relation to the shifts in research strategies to investigate multifactorial disorders (affected relative linkage designs, association strategies, and quantitative trait loci studies); new techniques and identified genetic mechanisms (expansion of trinucleotide repeats, genomic imprinting, mitochondrial DNA, fluorescent in-situ hybridisation, behavioural phenotypes, and animal models); and the successful localisation of genes.

Adolescent↗
PubMed1996

Modern molecular genetic approaches to complex traits: implications for psychiatric disorders.

The majority of common psychiatric disorders pose problems for geneticists because of their complex and non-Mendelian modes of inheritance. Early attempts to map genes for mental illness have so far largely overlooked this and sought genes of major effect in multiplex families using the lod score method of linkage analysis. However it seems that major genes are likely to be at best rare causes of common mental disorders, and the majority of cases probably reflect the interaction of several and perhaps many genes of comparatively small effect. There are two complementary sets of strategies that allow such genes to be identified. The first is to perform linkage analysis based on allele sharing in pairs of affected relatives. The second is to carry out association studies on samples of unrelated individuals. These methods and their applicability to psychiatric disorders are described. Psychiatric genetics has traditionally focussed on categorical phenotypes, but if valid continuous measures can be developed, powerful quantitative trait loci (QTL) approaches may also become feasible. Another important area is likely to be the study of relevant models in animals such as rodents in which genetic studies have many advantages. Finally we should not overlook the possibility that there are molecular explanations for irregular patterns of transmission such as mitochondrial inheritance, genomic imprinting and dynamic mutations.

Genetic Diseases, Inborn↗
PubMed2005

"A gene for...": the nature of gene action in psychiatric disorders.

A central phrase in the new "GeneTalk" is "X is a gene for Y," in which X is a particular gene on the human genome and Y is a complex human disorder or trait. This article begins by sketching the historical origins of this phrase and the concept of the gene-phenotype relationship that underlies it. Five criteria are then proposed to evaluate the appropriateness of the "X is a gene for Y" concept: 1) strength of association, 2) specificity of relationship, 3) noncontingency of effect, 4) causal proximity of X to Y, and 5) the degree to which X is the appropriate level of explanation for Y. Evidence from psychiatric genetics is then reviewed that address each of these criteria. The concept of "a gene for..." is best understood as deriving from preformationist developmental theory in which genes-like preformationist anlagen-"code for" traits in a simple, direct, and powerful way. However, the genetic contribution to psychiatric disorders fails to meet any of the five criteria for the concept of "X is a gene for Y." The impact of individual genes on risk for psychiatric illness is small, often nonspecific, and embedded in complex causal pathways. The phrase "a gene for..." and the preformationist concept of gene action that underlies it are inappropriate for psychiatric disorders.

Gene Expression Regulation↗
PubMed2002

[Mentalities and sterilization laws in Europe during the 1930s. Eugenics, genetics, and politics in a historic context].

The laws and related practice of sterilisation in Germany during the Nazi period (1933-1945) were not isolated phenomena. Rather, they have to be understood in the broader context of the eugenic and racial hygiene movement developing internationally during the first decades of the twentieth century. Central conditions allowing its emergence were scientific, sociopolitical, and cultural factors. Fears of biological degeneration, economic considerations, and trust in the future potential of biology and in particular genetics played a crucial role in many western societies. Eugenics and the practice of sterilisation are constitutively linked to scientific justifications, just as - complementarily - the development of genetics, in particular psychiatric genetics, is inextricably associated with eugenics and its funding by philanthropic or state institutions. Parallels and a multiplicity of mutual relations existed on various levels, in particular between Germany, the US, and Scandinavian countries.

Eugenics↗
PubMed2006

A preliminary comparison of the hopes of researchers, clinicians, and families for the future ethical use of genetic findings on schizophrenia.

A written questionnaire about genetic testing was distributed to all registrants at The 2004 World Congress of Psychiatric Genetics, mailed to clinical psychiatrists obtained from a directory of clinicians practicing in New York City, and mailed to members of families who have multiple affected family members with schizophrenia. A total of 274 individuals responded (162 researchers, 64 clinicians, and 48 family members). This survey shows that the majority of family members who completed the questionnaire (83.3%) would want to be tested if a genetic test were to become available. Over half of the family members (56.2%) would want prenatal testing. Similarly, over half of the clinicians (56.3%) would recommend it, despite only 25% of the researchers reporting that it would be a future useful tool. All of the clinicians surveyed thought adoption agencies should inform families about a family history of schizophrenia, while only half of the researchers thought this should be done (51.9%). These differences in opinions between consumers, their clinicians, and researchers could be based on a lack of understanding of the amount of risk conferred to family members by reported gene variants. Providing public discussions for placing these risks in perspective should be the responsibility of researchers. Open public discussion of the ethical and social uses of the information gained from psychiatric genetic research and its limitations is encouraged.

Adult↗
PubMed2002

Finding genes for bipolar disorder in the functional genomics era: from convergent functional genomics to phenomics and back.

Psychiatric genetics, while promising to unravel the mechanisms of psychiatric disorders, has proven to be a challenging field. Psychiatric disorders, like other common genetic traits, are complex and heterogeneous. Psychiatric genetics has also suffered from a lack of quantifiable, biology-based phenotypes. However, the field is currently at an opportune moment. The work of various investigators is on the verge of paying rich dividends. Efforts at positional cloning are being greatly accelerated by the fruits of the Human Genome Project. New tools of functional genomics, such as expression profiling and proteomics, are being applied to animal models. These two methods can complement each other in an approach we have termed convergent functional genomics. Lastly, improvements in the measurement of biologically distinct endophenotypes--or phenomic--will lead to a better understanding of the mapping of genes to phenotypes in both animal and human systems.

Journal Article↗
PubMed1999

Chromosome 22 workshop report.

The chromosome 22 workshop took place at the Sixth World Congress on Psychiatric Genetics from October 6th-10th, 1998 in Bonn, Germany. Aim of the workshop was to summarize the findings in psychiatric genetics on chromosome 22. Four reports concerning a susceptibility locus for schizophrenia and one report on bipolar disorder were given. A potential locus for nocturnal enuresis has been suggested to reside on chromosome 22.

Chromosome Mapping↗
PubMed2006

Resolving the paradox of common, harmful, heritable mental disorders: which evolutionary genetic models work best?

Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? We assess three leading explanations for this apparent paradox from evolutionary genetic theory: (1) ancestral neutrality (susceptibility alleles were not harmful among ancestors), (2) balancing selection (susceptibility alleles sometimes increased fitness), and (3) polygenic mutation-selection balance (mental disorders reflect the inevitable mutational load on the thousands of genes underlying human behavior). The first two explanations are commonly assumed in psychiatric genetics and Darwinian psychiatry, while mutation-selection has often been discounted. All three models can explain persistent genetic variance in some traits under some conditions, but the first two have serious problems in explaining human mental disorders. Ancestral neutrality fails to explain low mental disorder frequencies and requires implausibly small selection coefficients against mental disorders given the data on the reproductive costs and impairment of mental disorders. Balancing selection (including spatio-temporal variation in selection, heterozygote advantage, antagonistic pleiotropy, and frequency-dependent selection) tends to favor environmentally contingent adaptations (which would show no heritability) or high-frequency alleles (which psychiatric genetics would have already found). Only polygenic mutation-selection balance seems consistent with the data on mental disorder prevalence rates, fitness costs, the likely rarity of susceptibility alleles, and the increased risks of mental disorders with brain trauma, inbreeding, and paternal age. This evolutionary genetic framework for mental disorders has wide-ranging implications for psychology, psychiatry, behavior genetics, molecular genetics, and evolutionary approaches to studying human behavior.

Adaptation, Physiological↗
PubMed2004

Genomics and the Human Genome Project: implications for psychiatry.

In the past decade the Human Genome Project has made extraordinary strides in understanding of fundamental human genetics. The complete human genetic sequence has been determined, and the chromosomal location of almost all human genes identified. Presently, a large international consortium, the HapMap Project, is working to identify a large portion of genetic variation in different human populations and the structure and relationship of these variants to each other. The Human Genome Project has approached human genetics on a scale not previously seen in biology. This has been made possible by dramatic advances in high throughput technology and bio-informatics. Tools such as gene chips and micro-arrays have spawned an entirely new strategy to examine the function and expression of genes in a massively parallel fashion. Together these tools have dramatically advanced our knowledge about the human genome. They promise powerful new approaches to complex genetic traits such as psychiatric illness. The goals and progress of the Human Genome Project and the technology involved are reviewed. The implications of this science for psychiatric genetics are discussed.

Computational Biology↗