A family study of rapid-cycling bipolar illness

Nürnberger, John I.; Guroff, Juliet J.; Hamovit, Joel; Berrettini, Wade H.; Gershon, Elliot S.

doi:10.1016/0165-0327(88)90013-4

Cited by 56 publications

(27 citation statements)

References 11 publications

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“…Family studies of rapid cyclers show no increase in rapid cycling among relatives of rapid cycling versus nonrapid cycling bipolar patients (Nurnberger et al 1988). These data suggest that genetic factors do not play a role in determining which bipolar patients might become a rapid cycler.…”

Section: Areas For Future Researchmentioning

confidence: 79%

Bipolar Disorders in DSM-IV: Impact of Inclusion of Rapid Cycling as a Course Modifier

Dünner

1998

Neuropsychopharmacology

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Section: Areas For Future Researchmentioning

confidence: 79%

Bipolar Disorders in DSM-IV: Impact of Inclusion of Rapid Cycling as a Course Modifier

Dünner

1998

Neuropsychopharmacology

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“…Gershon et al observed an excess of major depression and schizoaffective disorder in the relatives of both mood disorder and schizophrenia probands. 80,81 The excess of major depression in relatives of both mood disorders and schizophrenia has been a consistent finding. 82 Studies from three data sets have addressed the issue of psychotic mood disorder/schizophrenia overlap.…”

Section: Systems Implicated In Parkinson's Disease and Schizophreniamentioning

confidence: 90%

Genetic tests of biologic systems in affective disorders

et al. 2005

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To liberate candidate gene analyses from criticisms of inexhaustiveness of examination of specific candidate genes, or incompleteness in the choice of candidate genes to study for specific neurobiological pathways, study of sizeable sets of genes pertinent to each putative pathophysiological pathway is required. For many years, genes have been tested in a 'one by one' manner for association with major affective disorders, primarily bipolar illness. However, it is conceivable that not individual genes but abnormalities in several genes within a system or in several neuronal, neural, or hormonal systems are implicated in the functional hypotheses for etiology of affective disorders. Compilation of candidate genes for entire pathways is a challenge, but can reasonably be carried out for the major affective disorders as discussed here. We present here five groupings of genes implicated by neuropharmacological and other evidence, which suggest 252 candidate genes worth examining. Inexhaustiveness of gene interrogation would apply to many studies in which only one polymorphism per gene is analyzed. In contrast to whole-genome association studies, a study of a limited number of candidate genes can readily exploit information on genomic sequence variations obtained from databases and/or resequencing, and has an advantage of not having the complication of an extremely stringent statistical criterion for association. Molecular Psychiatry (2005) 10, 719-740.

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“…This notion is compatible with previous research on rapid cycling, which showed that the morbid risk for affective disorder is not different in the relatives of rapid cycling and nonrapid cycling probands. [20][21][22] These same studies have produced inconclusive results regarding the prevalence of rapid cycling in the relatives of bipolar patients with and without the rapid cycling form. In the presence of a relatively modest genetic effect, as suggested by our results, these studies had a low power to demonstrate a significant genetic effect.…”

mentioning

confidence: 99%

“…Other factors that have been suggested are female gender [20][21][22] and the presence of thyroid disorder. 23 Exposure to tricyclic antidepressants has been consistently reported to induce rapid cycling.…”

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confidence: 99%

Low activity allele of catechol-O-methyltransferase gene associated with rapid cycling bipolar disorder

et al. 1998

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Catechol-O-methyltransferase (COMT) plays a major role in the breakdown of catecholamines.1 An amino acid polymorphism (val-108-met) determines high and low activity of the enzyme.2,3 A recent study in a small sample of patients with velo-cardio-facial syndrome who had bipolar affective disorder suggested that the Met (low activity) COMT allele might be associated with rapid-cycling in this population. 4 We therefore tested the hypothesis that the Met allele might be associated with rapid cycling bipolar disorder in the wider population. We studied a sample of British Caucasian DSM-IV bipolar patients, of whom 55 met criteria for rapid cycling at some time during the illness and 110 met stringent criteria for a definite non-rapid cycling course. The COMT genotype was determined using a PCR assay. The low activity allele was more frequent in the group of rapid cyclers: 0.55 vs 0.42 (one-tailed 2 = 5.12, d.f. = 1, P = 0.012), and bearers of low activity alleles showed a dose-dependent increased risk of lifetime occurrence of rapid cycling: 2 test of linear association = 4.84, d.f. = 1, P = 0.014. Our data support the hypothesis that variation in the COMT gene modifies the course of bipolar disorder.

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A family study of rapid-cycling bipolar illness

Cited by 56 publications

References 11 publications

Bipolar Disorders in DSM-IV: Impact of Inclusion of Rapid Cycling as a Course Modifier

Bipolar Disorders in DSM-IV: Impact of Inclusion of Rapid Cycling as a Course Modifier

Genetic tests of biologic systems in affective disorders

Low activity allele of catechol-O-methyltransferase gene associated with rapid cycling bipolar disorder

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