Genetic aetiology of mood disorders

Author(s):  
Pierre Oswald ◽  
Daniel Souery ◽  
Julien Mendlewicz

Advances towards the understanding of the etiological mechanisms involved in mood disorders provide interesting yet diverse hypotheses and promising models. In this context, molecular genetics has now been widely incorporated into genetic epidemiological research in psychiatry. Affective disorders and, in particular, bipolar affective disorder (BPAD) have been examined in many molecular genetic studies which have covered a large part of the genome, specific hypotheses such as mutations have also been studied. Most recent studies indicate that several chromosomal regions may be involved in the aetiology of BPAD. Other studies have reported the presence of anticipation in BPAD and in unipolar affective disorder (UPAD). In parallel to these new developments in molecular genetics, the classical genetic epidemiology, represented by twin, adoption and family studies, provided additional evidence in favour of the genetic hypothesis in mood disorders. Moreover, these methods have been improved through models to test the gene-environment interactions. In addition to genetic approaches, psychiatric research has focused on the role of psychosocial factors in the emergence of mood disorders. In this approach, psychosocial factors refer to the patient's social life context as well as to personality dimensions. Abnormalities in the social behavior such as impairment in social relationships have been observed during episode of affective disorders, and implicated in the etiology of affective disorders. Further, gender and socio-economic status also emerged as having a possible impact on the development of affective disorders. Finally, the onset and outcome of affective disorders could also be explained by interactions between the social life context and the individual's temperament and personality. The importance of temperament and personality characteristics in the etiology of depression has been emphasized in various theories, although disagreement exists with regard to terminology and the etiology. While significant advances have been done in these two major fields of research, it appears that integrative models, taking into account the interactions between biological (genetic) factors and social (psychosocial environment) variables offer the most reliable way to approach the complex mechanisms involved in the etiology and outcome of mood disorders. This chapter will review some of the most promising genetic and psychosocial hypotheses in mood disorders that can be integrated in interactive models.

1997 ◽  
Vol 12 (S2) ◽  
pp. 63s-69s ◽  
Author(s):  
D Souery ◽  
O Lipp ◽  
B Mahieu ◽  
J Mendlewicz

SummaryThe present article reviews the recent molecular genetic findings in affective disorders. Results of linkage and association studies are discussed in regard to the main limitations of these approaches in psychiatric disorders. On the whole, linkage and association studies contributed to the localisation of some potential vulnerability genes for Bipolar affective disorder on chromosomes 18, 5, 11, 4, 21 and X. The hypothesis of anticipation in affective disorders is also considered in light of interesting results with trinucleotide repeat mutations.


1997 ◽  
Vol 9 (2) ◽  
pp. 52-54
Author(s):  
D. Souery ◽  
J. Mendlewicz

Molecular genetics has now been widely incorporated into genetic epidemiological research in psychiatry. Affective disorders and, in particular, bipolar affective disorder (BPAD) have been examined in many molecular genetic studies which have covered a large part of the genome. Specific hypotheses such as mutations have also been studied. Most recent studies indicate that several chromosomal regions may be involved in the aetiology of BPAD. These include genes on chromosomes 18, 21, 4, 5, 11 and X. Other studies have reported the presence of anticipation in BPAD and in unipolar affective disorder (UPAD). This phenomenon describes the increase in clinical severity and decrease in age of onset observed in successive generations. This mode of transmission correlates with the presence of specific mutations (trinucleotide repeat sequences). Associations with these mutations have been reported in different populations of BPAD-patients and may represent a genetic factor involved in the transmission of the disorder.These findings are all preliminary and require to be confirmed. Large multi-centres and multi-disciplinary projects are currently underway in Europe and in the US and hopefully will improve our understanding of the genetic factors involved in affective disorders. In addition, genetic approaches used in psychiatry are being combined with an assessment of non-genetic susceptibility factors. The investigation of interactions between gene and environment is one of the most promising areas dealing with complex multi-factorial diseases such as the affective disorders.


2000 ◽  
Vol 12 (3) ◽  
pp. 65-68 ◽  
Author(s):  
D. Souery ◽  
I. Massat ◽  
J. Mendlewicz

ABSTRACTAdvances towards the understanding of the etiological mechanisms involved in mood disorders provide interesting yet diverse hypotheses and promising models. In this context, molecular genetics has now been widely incorporated into genetic epidemiological research in psychiatry. Affective disorders and, in particular, bipolar affective disorder (BPAD) have been examined in many molecular genetic studies which have covered a large part of the genome, specific hypotheses such as mutations have also been studied. Most recent studies indicate that several chromosomal regions may be involved in the aetiology of BPAD. Other studies have reported the presence of anticipation in BPAD. This phenomenon describes the increase in clinical severity and decrease in age of onset observed in successive generations. This mode of transmission correlates with the presence of specific mutations (Trinucleotide Repeat Sequences) and may represent a genetic factor involved in the transmission of the disorder. In parallel to these new developments in molecular genetics, the classical genetic epidemiology, represented by twin, adoption and family studies, provided additional evidence in favour of the genetic hypothesis in mood disorders. Moreover, these methods have been improved through models to test the gene-environment interactions. While significant advances have been made in this major field of research, it appears that integrative models, taking into account the interactions between biological (genetic) factors and social (psychosocial environment) variables offer the most reliable way to approach the complex mechanisms involved in the etiology and outcome of mood disorders.


2009 ◽  
Vol 2 (2) ◽  
pp. 92-105 ◽  
Author(s):  
Ueli Kramer ◽  
Guy Bodenmann ◽  
Martin Drapeau

AbstractThe construct of cognitive errors is clinically relevant for cognitive therapy of mood disorders. Beck's universality hypothesis postulates the relevance of negative cognitions in all subtypes of mood disorders, as well as positive cognitions for manic states. This hypothesis has rarely been empirically addressed for patients presenting bipolar affective disorder (BD). In-patients (n= 30) presenting with BD were interviewed, as were 30 participants of a matched control group. Valid and reliable observer-rater methodology for cognitive errors was applied to the session transcripts. Overall, patients make more cognitive errors than controls. When manic and depressive patients were compared, parts of the universality hypothesis were confirmed. Manic symptoms are related to positive and negative cognitive errors. These results are discussed with regard to the main assumptions of the cognitive model for depression; thus adding an argument for extending it to the BD diagnostic group, taking into consideration specificities in terms of cognitive errors. Clinical implications for cognitive therapy of BD are suggested.


Author(s):  
E. D. Kasyanov ◽  
G. E. Maso ◽  
A. O. Kibitov

Affective disorders (recurrent depressive disorder and bipolar affective disorder) are multifactorial and polygenic diseases, which suggests the involvement of multiple neurobiological mechanisms. The phenotype of affective disorders is a heterogeneous group of clinically similar psychopathological symptoms, which also makes it difficult to detect potential biomarkers and new therapeutic targets. To study families at high risk of developing affective disorders using both clinical and molecular genetic approaches can help to study the neurobiological basis of depressive conditions, as well as to identify endophenotypes of affective disorders. The most important criterion for an endophenotype is its heritability, which can be proved only within the framework of the family design of the study. Comprehensive clinical and molecular genetic studies based on family design have the best prospects.


1999 ◽  
Vol 11 (2) ◽  
pp. 67-70
Author(s):  
D. Souery ◽  
J. Mendlewicz

Traditional methods used to asses genetic effects, such as twins, adoption and family studies, have demonstrated the role genetic vulnerability factors in the etiology of major psychiatric diseases such as affective disorders and schizophrenia. It remains however impossible, using these methods, to specify the genetic variables involved and the exact mode of transmission of these diseases. New genetic approaches in psychiatry include the use of DNA markers in sophisticated strategies to examine families and populations. Genetic linkage (in families) and allelic association (in unrelated subjects) are the most frequent techniques applied searching for genes in psychiatric diseases. Advances in these methods have permitted their application to complex diseases in which the mode of genetic transmission is unknown. Affective disorders and, in particular, bipolar affective disorder (BPAD) have been examined in many molecular genetic studies which have covered a large part of the genome, specific hypotheses such as mutations have also, been studied. Most recent studies indicate that several chromosomal regions may be involved in the aetiology of affective disorders. Large multi-centre and multi-disciplinary projects are currently underway in Europe and in the US and hopefully will improve our understanding of the genetic factors involved in affective disorders. In parallel to these new developments in molecular genetics, the classical genetic epidemiology, represented by twin, adoption and family studies, have been improved, providing validated models to test the gene-environment interactions.


2007 ◽  
Vol 190 (1) ◽  
pp. 6-10 ◽  
Author(s):  
Sanne G. H. A. Swinnen ◽  
Jean-Paul Selten

BackgroundMigration is a risk factor for the development of schizophrenia.AimsTo examine whether migration is also a risk factor for bipolar affective disorder, unipolar depressive disorder and mood disorders in general.MethodMedline was searched for population-based incidence studies concerning mood disorders among migrants and mean relative risks were computed using a mixed-effects statistical model.ResultsOnly a few studies of unipolar depressive disorder were retrieved. The mean relative risk of developing bipolar affective disorder among migrants was 2.47 (95% C11.33–4.59). However, after excluding people of African-Caribbean origin in the UK this risk was no longer significantly increased. The mean relative risk of mood disorders of unspecified polarity was 1.25 (95% CI 1.04–1.49) and that of any mood disorder was 1.38 (95% CI 1.17–1.62).ConclusionsThere is no conclusive evidence for a large increase in the risk of mood disorders associated with migration.


1977 ◽  
Vol 40 (3_suppl) ◽  
pp. 1135-1141 ◽  
Author(s):  
Donald S. Schaeffer

Patients in an affective disorders clinic diagnosed unipolar ( n = 13), bipolar ( n = 10), or schizo-affective ( n = 7) disorder were given a Maudsley Neuroticism Scale, a Rorschach, and a form interview. Mood over the course of the procedure was assessed and speech content measured. Diagnostic groups differed on background measures of social competence, schizo-affectives being poorer than bipolar and unipolar subjects. Rorschach pathognomic verbalization scores for schizo-affective and bipolar subjects were poorer than for unipolar subjects. Rorschach form definiteness for schizo-affectives was poorer than for bipolar and unipolar subjects. Neuroticism scores did not discriminate diagnostic groups but correlated with mood ratings. History of mania was associated with symbolic bizarreness, resembling schizo-affective disorder. However, the social competence and perceptual maturity of subjects with manic histories did not differ from those without.


1992 ◽  
Vol 7 (4) ◽  
pp. 153-159
Author(s):  
O Halfon ◽  
MC Mouren-Simeoni ◽  
F Radat ◽  
E Albert ◽  
V Nahama ◽  
...  

SummaryThe prognostic significance of an index episode of affective disorder with delusions was assessed in a longitudinal study of a cohort of adolescent psychiatric inpatients (n = 43). Part I of a study has been reported in a previous article. Initial assessmentdata (anamnestic variables, clinical assessment) did not discriminate between onset of affective disorder and schizophrenia. Part II of the study provides a longitudinal perspective of the cohort's diagnostic and life adjustment: diagnoses of schizophrenia increased, schizophreniform disorders disappeared, affective disorders were stable and a schizo-affective category emerged. Patients in the schizophrenic category had severely impaired life adjustment, while the level of functioning in unipolar and bipolar patients was consistently satisfactory. Compared to the initial diagnosis, the cohort showed a tendency to develop into schizophrenia. It is too early to affirm that every adolescent with delusional symptoms at onset will later develop schizophrenia, however, this risk appears real.


2000 ◽  
Vol 12 (3) ◽  
pp. 99-103 ◽  
Author(s):  
T. Lloyd ◽  
P.B. Jones

ABSTRACTThe past 20 years have seen much research into affective disorders, reflecting advances in both pharmacological and psychological treatments. However, there has been little basic epidemiological research into bipolar illness. This is particularly apparent regarding its basic occurrence and possible epigenetic causes. This presentation will attempt to bring together and integrate the available evidence regarding the basic epidemiology of bipolar disorder, define areas where further research is needed, and outline a large epidemiological study including bipolar affective disorder that has been supported by the Stanley Foundation.


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