Abstract
Background: The available evidence for an involvement of the heterotrimeric guanine-nucleotide-binding proteins (G proteins) in bipolar disorder relies primarily on the effects of lithium salts on G protein function and on alterations in the concentration or function of G proteins (most notably G(s)-α) in peripheral leukocytes and in postmortem tissues of patients with bipolar disorder. Methods: The hypothesis that a mutation in G(s)-α gene confers an increased susceptibility to bipolar disorder was tested by the following strategies: (1) mutational screening of the G(s)-a subunit gene coding sequences and promoter sequences by denaturing gradient gel electrophoresis in unrelated individuals with bipolar disorder and (2) association and linkage analyses with a common silent exonic polymorphism, using genetic allelic information from American families with at least 1 affected child. For association analysis, the transmission test for linkage disequilibrium was used; for linkage analysis, non-parametric methods were used. Results: No structural or regulatory mutations in this gene were found in bipolar disorder; the results of association and genetic linkage were negative. Conclusion: Our results do not support the speculation that the G(s)-α protein gene has a role in the genetic predisposition to bipolar disorder.
Original language | English |
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Pages (from-to) | 44-48 |
Number of pages | 5 |
Journal | Archives of General Psychiatry |
Volume | 54 |
Issue number | 1 |
DOIs | |
State | Published - 1 Jan 1997 |
ASJC Scopus subject areas
- Arts and Humanities (miscellaneous)
- Psychiatry and Mental health