The Etiology of Manic-Depressive Syndromes With Special Reference to Their Occurrence in Twins

Rosanoff, Aaron J.; Handy, Leva M.; Plesset, Isabel Rosanoff

doi:10.1176/ajp.91.4.725

Cited by 134 publications

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“…Our findings suggest that the GABRA3 polymorphism may confer susceptibility to or may be in linkage disequilibrium with another gene involved in the genetic etiology of BPAD. The hypothesis that bipolar affective disorder (BPAD) is transmitted through a gene on the X-chromosome was first proposed by Rosanoff et al in 1935. 1 Several linkage studies have investigated the region Xq26-28 in BPAD (see Table 1).…”

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“…The hypothesis that bipolar affective disorder (BPAD) is transmitted through a gene on the X-chromosome was first proposed by Rosanoff et al in 1935. 1 Several linkage studies have investigated the region Xq26-28 in BPAD (see Table 1). Among them, the largest pedigree series reported a high Lod score (z) confirming linkage (z = 8.1 at = 0.15) to color blindness (CB) in 17 North American families.…”

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Excess of allele1 for α3 subunit GABA receptor gene (GABRA3) in bipolar patients: a multicentric association study

et al. 2002

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The available data from preclinical and pharmacological studies on the role of gamma amino butyric acid (GABA) support the hypothesis that a dysfunction in brain GABAergic system activity contributes to the vulnerability to bipolar affective disorders (BPAD). Moreover, the localization of the ␣3 subunit GABA receptor GABRA3 gene on the Xq28, a region of interest in certain forms of bipolar illness, suggests that GABRA3 may be a candidate gene in BPAD. In the present study, we tested the genetic contribution of the GABRA3 dinucleotide polymorphism in a European multicentric case-control sample, matched for sex and ethnogeographical origin. Allele and genotype (in females) frequencies were compared in 185 BPAD patients and 370 controls. A significant increase of genotype 1-1 was observed in BPAD females compared to controls (P = 0.0004). Furthermore, when considering recessivity of allele 1 (females with genotype 1-1 and males carrying allele 1), results were even more significant (P = 0.00002). Our findings suggest that the GABRA3 polymorphism may confer susceptibility to or may be in linkage disequilibrium with another gene involved in the genetic etiology of BPAD.

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Excess of allele1 for α3 subunit GABA receptor gene (GABRA3) in bipolar patients: a multicentric association study

et al. 2002

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“…On any hypothesis, the relatively greater incidence of affective psychoses in the female than in the male requires explanation. Rosanoff et al (1935) first suggested that an X-linked dominant gene is involved and this was later suggested by a statistical experts (Burch 1964), who also noted that statistical features of the disorder closely resembled comparable features of diseases that were -27 -widely believed to have an auto-immune aetiology. Several studies have suggested the possibility of a single dominant gene located on the X-chromosome in the bipolar group (Reich et al 1969;Winokur and Tanna 1969;Mendlewicz et al 1972a;Mend.lewicz and Rainer 1974).…”

Section: Epidemiology Of Denressionmentioning

confidence: 97%

Depression in Patients With Epilepsy

Robertson¹

1984

Clinical Neuropharmacology

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“…The idea that X linkage may explain some forms of aVective disorder goes back over half a century 61 and has been debated vigorously over the last 25 years because of several reports of families showing cosegregation between X linked markers (such as colour blindness or glucose-6-phosphate dehydrogenase deficiency) and bipolar disorder, suggesting the possibility of an X linked dominant susceptibility gene. [62][63][64] However, these reports have been criticised on methodological grounds, 65 particular problems being ascertainment bias and non-blinding to marker status.…”

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Genetics of bipolar disorder

Craddock¹,

Russell²

2006

Beyond Nature and Nurture in Psychiatry

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Bipolar disorder (also known as manic depressive illness) is a complex genetic disorder in which the core feature is pathological disturbance in mood (aVect) ranging from extreme elation, or mania, to severe depression usually accompanied by disturbances in thinking and behaviour. The lifetime prevalence of 1% is similar in males and females and family, twin, and adoption studies provide robust evidence for a major genetic contribution to risk. There are methodological impediments to precise quantification, but the approximate lifetime risk of bipolar disorder in relatives of a bipolar proband are: monozygotic co-twin 40-70%; first degree relative 5-10%; unrelated person 0.5-1.5%. Occasional families may exist in which a single gene plays the major role in determining susceptibility, but the majority of bipolar disorder involves the interaction of multiple genes (epistasis) or more complex genetic mechanisms (such as dynamic mutation or imprinting). Molecular genetic positional and candidate gene approaches are being used for the genetic dissection of bipolar disorder. No gene has yet been identified but promising findings are emerging. Regions of interest identified in linkage studies include 4p16, 12q23-q24, 16p13, 21q22, and Xq24-q26. Chromosome 18 is also of interest but the findings are confusing with up to three possible regions implicated. To date most candidate gene studies have focused on neurotransmitter systems influenced by medication used in clinical management of the disorder but no robust positive findings have yet emerged. It is, however, almost certain that over the next few years bipolar susceptibility genes will be identified. This will have a major impact on our understanding of disease pathophysiology and will provide important opportunities to investigate the interaction between genetic and environmental factors involved in pathogenesis. This is likely to lead to major improvements in treatment and patient care but will also raise important ethical issues that will need to be addressed. (J Med Genet 1999;36:585-594)

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The Etiology of Manic-Depressive Syndromes With Special Reference to Their Occurrence in Twins

Cited by 134 publications

References 0 publications

Excess of allele1 for α3 subunit GABA receptor gene (GABRA3) in bipolar patients: a multicentric association study

Excess of allele1 for α3 subunit GABA receptor gene (GABRA3) in bipolar patients: a multicentric association study

Depression in Patients With Epilepsy

Genetics of bipolar disorder

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