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At least 19 recordsLinked to original sources
PubMed1987

Psychiatric genetics and psychiatric nosology.

At the present time, family and twin data are used in psychiatry to test clinical concepts at issue, and, in particular, to validate or reject diagnostic classifications. The dichotomy between the schizophrenias and the effective disorders, as suggested by Kraepelin, has been supported by contemporary family and twin studies and also is corroborated by modern family and adoption studies. In the atypical psychoses it is demonstrated impressively how family data vary with different sampling procedures and diagnostic practices. In the affective disorders, the family findings at first favored the separation of unipolar and bipolar disorders but, subsequently, this concept was questioned and revised. Currently, psychiatric genetics attempts to contribute to the understanding of the affective disorders, in particular the depressions, by delineating subgroups and by looking for possible genetic relations between depression and frequently associated disorders, such as anxiety or anorexia.

Affective Disorders, Psychotic↗
PubMed1985

Controversies and consistencies in psychiatric genetics.

The methodology in psychiatric genetics, including family studies, twin studies, and adoption strategies, developed during the last 70 years to a high degree of perfection, has established beyond doubt the heritability of the major psychoses, the schizophrenic and manic-depressive disorders. In spite of recent refinements, including twin-family-study strategies, dual mating strategies, and advanced mathematical models and statistics the mode of inheritance is still undetermined. Evidence for heterogeneity in both schizophrenia and manic-depressive psychosis has been brought up leading to new approaches in diagnostic delimitations. However, the final solution of this issue probably has to await the finding of a genetic marker, for which recent advances in molecular biology as seen in Huntington's disease may give some hope.

Adoption↗
PubMed2026

Can Psychiatric Genetics Advance Without Incorporating a Life Course Perspective?

Psychiatric disorders unfold over the life course; however, genomic studies of these conditions overwhelmingly rely on phenotypes collected at a single time point, often in adulthood. Therefore, genome-wide association studies (GWASs) of psychiatric conditions may miss genetic variants with time-varying relevance to etiology, prevention, and treatment, such as those that influence trajectories of symptoms and behaviors, age at onset, course of treatment response, and the co-evolution of comorbidities. With recent advances in longitudinal biobanks and analytic tools, we posit that incorporating a life course perspective in psychiatric genetics will enable critically relevant insights into each of these areas of investigation. We propose that the current inconsistent portability of polygenic scores across age groups can be reconciled through the design of carefully considered longitudinal GWASs in age-diverse samples. Pioneering longitudinal GWASs in psychiatry have revealed novel genomic signals associated with time-dependent phenotypes that are distinct from those influencing lifetime diagnosis, suggesting that the study of longitudinal phenotypes will complement cross-sectional approaches and empower biological and therapeutic discoveries. Advances in post-GWAS functional annotation resources and analytic approaches now enable us to contextualize the genetic contributions to psychiatric disorders as dynamic age- and exposure-dependent processes. Although longitudinal GWASs pose unique challenges with regard to data availability, selection bias, and missing data, integrating temporality into psychiatric genetics at scale is now attainable and promises to reveal novel biology and therapeutic opportunities for psychiatric conditions.

Cohort study↗
PubMed1992

Psychiatric, genetic, and positron emission tomographic evaluation of persons at risk for Huntington's disease.

We examined chorea-free subjects at risk for Huntington's disease (n = 52) for lifetime psychiatric diagnoses, present mood, genetic marker status, and caudate glucose metabolic rates with positron emission tomography. Based on previous work, a caudate-ipsilateral hemisphere ratio less than 1.15 was defined as abnormal and predictive of Huntington's disease. None of three methods used to segregate subjects into groups more and less likely to develop Huntington's disease gave significant group rate differences for any formal psychiatric diagnoses. On present mood testing, however, subjective "anger/hostility" was significantly higher in those likely, compared with those less likely, to develop Huntington's disease, as determined by all three methods.

Adult↗
PubMed1986

Clinical methods in psychiatric genetics. II. The high risk approach.

The study of individuals at "high" risk for developing psychiatric disorders is useful in confirming that a biological trait marker identified in patient populations is also present in genetically susceptible individuals who have never been ill, and predicts the future onset of illness. We outline a systematic method for deciding which variables to choose and how many individuals are required in order for a study to have sufficient power. We demonstrate how these decisions depend on the assumptions that can be made with regard to the mode of inheritance of the biological trait, the relationship of the biological trait to illness, and the magnitude of the mean difference observed between patients and controls. We also quantify the increased power of studying offspring of two affected parents rather than offspring of one affected parent.

Affective Disorders, Psychotic↗
PubMed1975

Some recent developments in psychiatric genetics.

The methods and results of some recent family, twin and adoption studies of childhood behaviour disorders, crime, alcoholism, psychopathic personality and neurosis are briefly described. The data of Slater (1938) on the parents and children of manic-depressives are reanalysed. Bipolar affective illness were more frequent in the families of bipolar than unipolar probands. There was no support for sex-linked inheritance in either group or for further genetic subdivision of the unipolar group according to age of onset or alcoholic or psychopathic family history. It is suggested that for the time being we may have to be satisfied with three broad and aetiologically overlapping clinical types of depression: bipolar, unipolar and reactive.

Adoption↗
PubMed1986

Clinical methods in psychiatric genetics. III. Environmental stratification may simulate a genetic effect in adoption studies.

In adoption studies, the possibility of inadvertent matching between biological and adoptive parents for some environmental variable (known or unknown) correlated with illness must be considered. We examine such bias quantitatively and show how a genetic effect can be simulated. Existence of a genetic effect which is independent of environmental correlation can be accepted, when the frequency of a disease in adoptees who have a biological parent affected and no adoptive parents affected is significantly greater than the frequency of the disease in adoptees who have an adopted parent affected and no biological parents affected. The published data on schizophrenia, alcoholism, and criminality do not exclude the possibility of undetected environmental correlations simulating a genetic effect, according to this direct criterion.

Adoption↗
PubMed1986

Clinical methods in psychiatric genetics. I. Robustness of genetic marker investigative strategies.

Population stratification, secondary effects of illness or treatment, biological heterogeneity of a clinical syndrome, or complex biology underlying a syndrome (where only one component is measured) are conditions which may obscure the association of a genetic risk factor with a clinical syndrome. We consider several investigative strategies under each of these conditions. Only segregation-based paradigms are robust to genetic heterogeneity and population stratification. But secondary effects on the risk factor produced by illness or treatment require other strategies for their detection.

Chromosome Aberrations↗
PubMed1990

[Historic, social psychiatric, genetic and anthropologic aspects of turricephaly].

At first estimations of turricephaly from antiquity till modern times are exhibited and at last also results of own examination of over an average disturbed social behaviour and constitutional biological aspects of patients with turricephaly. The dominant inheritance of turricephaly and also peristatic and influences of races in the genesis of premature craniosyntosis are viewed by current literature.

Child↗