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No Abnormality in the Gene for the G Protein Stimulatory α Subunit in Patients With Bipolar Disorder

Anca Ram, MD; Françoise Guedj, MD; Anibal Cravchik, MD, PhD; Lee Weinstein, MD; Qiuhe Cao, MD; Judith A. Badner, MD, PhD; Lynn R. Goldin, PhD; Nimrod Grisaru, MD; Husseini K. Manji, MD; Robert H. Belmaker, MD; Elliot S. Gershon, MD; Pablo V. Gejman, MD
Arch Gen Psychiatry. 1997;54(1):44-48. doi:10.1001/archpsyc.1997.01830130048010.
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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 Gs-α) in peripheral leukocytes and in postmortem tissues of patients with bipolar disorder.

Methods:  The hypothesis that a mutation in Gs-α gene confers an increased susceptibility to bipolar disorder was tested by the following strategies: (1) mutational screening of the Gs-α 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 Gs-α protein gene has a role in the genetic predisposition to bipolar disorder.


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