Association of the Dysbindin Gene With Bipolar Affective Disorder

• Published in: The American journal of psychiatry Vol. 163; no. 9; pp. 1636 - 1638
• Main Authors: Breen, Gerome, Prata, Diana, Osborne, Sarah, Munro, Janet, Sinclair, Maggie, Li, Tao, Staddon, Susan, Dempster, David, Sainz, Ricardo, Arroyo, Barbara, Kerwin, Robert W., St. Clair, David, Collier, David
• Format: Journal Article
• Language: English
• Published: Washington, DC American Psychiatric Association 01-09-2006
• Subjects: Adult and adolescent clinical studies; Biological and medical sciences; Bipolar disorder; Bipolar Disorder - genetics; Bipolar disorders; Carrier Proteins - genetics; Case-Control Studies; Dysbindin; Dystrophin-Associated Proteins; Genes; Genetic Markers; Genetic Predisposition to Disease; Genotype; Haplotypes; Humans; Medical sciences; Models, Genetic; Mood disorders; Phenotype; Polymorphism, Single Nucleotide - genetics; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Risk Factors; Schizophrenia; Schizophrenia - genetics; Affective disorder; Mood disorder; Genetics; Bipolar disorder; Gene; Genetic determinism
• ISSN: 0002-953X; 1535-7228
• DOI: 10.1176/ajp.2006.163.9.1636

Objective:
In the study of bipolar affective disorder and schizophrenia, there is some evidence suggesting a phenotypic and genetic overlap between the two disorders. A possible link between bipolar affective disorder and schizophrenia remains arguable, however. The authors hypothesized that dysbindin, which is a probable susceptibility gene for schizophrenia, was associated with bipolar affective disorder and tested this hypothesis using a case-control design study.
Method:
Participants included 213 patients with bipolar I disorder and 197 comparison subjects. In each subject, 10 polymorphisms in the dysbindin gene were genotyped and assessed.
Results:
Two polymorphisms showed individual genotypic association with bipolar I disorder. Multiple marker haplotypes were more strongly associated, with the rarer of the two common haplotypes being overrepresented in the patients with bipolar affective disorder. A similar finding was reported in patients with schizophrenia in a previous study.
Conclusions:
Findings suggest that the human dysbindin gene may play a role in the susceptibility to bipolar affective disorder, which underscores a potentially important area of etiological overlap with schizophrenia. The existence of shared genetic risk factors will, in time, lead to changes in the current nosology of major psychoses.