Mapping genes for manic-depression and schizophrenia with DNA markers

Byerley, William; Mellon, Charles David; O’Connell, P.; Jean-Marc,; Lalouel,; Yusuke,; Nakamura,; Leppert, M.; White, Ray

doi:10.1016/0166-2236(89)90134-3

Cited by 10 publications

(3 citation statements)

References 27 publications

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“…The chromosomal areas suggested in this review are consistent with those indicated by other authors (Byerley et at, 1989;DeLisi & Lovett, 1990;Diehl & Kendler, 1989) as of potential interest for schizophrenia. Published results of linkage studies of schizophrenia have focused on chromosome 5.…”

Section: Discussionsupporting

confidence: 73%

Chromosomal Aberrations and Schizophrenia

Bassett

1992

Br J Psychiatry

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Chromosomal aberrations associated with schizophrenic disorders may suggest regions in which to focus a search for genes predisposing to schizophrenia by a linkage strategy. As for other genetic illnesses, chromosomal abnormalities may also provide useful tools for subsequent physical mapping, fine localisation, and isolation of important susceptibility genes. Identification of several chromosomal aberrations may be especially important, given the unknown pathophysiology, the paucity of known brain genes, and the probable genetic heterogeneity of schizophrenia and manic-depression. However, because psychiatric disorders are common and inherited in a complex manner, researchers must use caution when drawing inferences about associations with chromosomal aberrations. Reported abnormalities involving autosomes (chromosomes 1 -22) associated with psychotic disorders are reviewed. Their relevance to linkage studies localising genes for schizophrenia was estimated by standardised criteria for specificity, diagnosis, family history, and overall weight of evidence. Four 'possibly relevant' chromosomal regions were identified: 5q, 11q, 18q, and 19p. This paper outlines strategies for future studies to detect new chromosomal aberrations associated with major psychotic disorders that may be relevant to isolating the genes for schizophrenia.

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Section: Discussionsupporting

confidence: 73%

Chromosomal Aberrations and Schizophrenia

Bassett

1992

Br J Psychiatry

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“…Despite our precautions of strict geographical inclusion criteria for the selection of subjects, and minimization of type I errors with matching and statistical tools applying to the paired‐samples, we cannot completely exclude a type I error related to population stratification. Regarding the DRD2 gene, overall the literature reports negative linkage results in BPAD [Byerley et al, 1989; Holmes et al, 1991; Pakstis et al, 1991; Mitchell et al, 1992; Nothen et al, 1992; Nanko et al, 1994; De bruyn et al, 1994, Ewald et al, 1995; 1996; Grassi et al, 1996; Serretti et al, 2000], except for three studies, the first reported a balanced t9;11 chromosomal translocation that cosegregated with BPAD close to the site of DRD2 in one family [Smith et al, 1989]. The second study reported a translocation breakpoint in the same region of chromosome 11 that segregated with mental illnesses including BPAD [St. Clair et al, 1990].…”

Section: Discussionmentioning

confidence: 99%

Positive association of dopamine D2 receptor polymorphism with bipolar affective disorder in a European multicenter association study of affective disorders

et al. 2002

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Convincing evidence for a genetic component in the etiology of affective disorders (AD), including bipolar affective disorder (BPAD) and unipolar affective disorder (UPAD), is supported by traditional and molecular genetic studies. Most arguments lead to the complex inheritance hypothesis, suggesting that the mode of inheritance is probably not Mendelian but most likely oligogenic (or polygenic) and that the contribution of genes could be moderate or weak. The purpose of the present European multicenter study (13 centers) was to test the potential role in BPAD and UPAD of two candidate dopaminergic markers, DRD2 and DRD3, using a case-control association design. The following samples were analyzed for DRD2: 358 BPAD/358 control (C) and 133 UPAD/ 133 C subjects, and for DRD3: 325 BPAD/ 325 C and 136 UPAD/136 C subjects. Patients and controls were individually matched for sex, age ( plus minus five years) and geographical origin. Evidence for significant association between BPAD and DRD2 emerged, with an over-representation of genotype 5-5 (P=0.004) and allele 5 (P=0.002) in BPAD cases compared to controls. No association was found for DRD2 in UPAD, and for DRD3 neither in BPAD or UPAD. Our results suggest that the DRD2 microsatellite may be in linkage disequilibrium with a nearby genetic variant involved in the susceptibility to BPAD. Our large European sample allowed for replicating of some previous reported positive findings obtained in other study populations.

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“…Thus, depending on the conditions, the very same allele may at one time result in a sample of phenotypes with a high degree of heritability, and another time in a sample characterized by much environmentally dependent variability. It would seem that the ongoing debate and conflicting results on the heritability of schizophrenia (Byerley et al 1989;Kennedy et al 1988;McGue et al 1983) may in part reflect such interac-tion between gene effects and developmental properties of the brain (Lyon et al 1989). If this scenario is correct, there is obviously no logical way to disentangle hereditary and environmental contributions to a particular behavioral phenotype, and the results of the classical partitioning by means of ANOVA are meaningless, certainly for predicting the behavior of an individual, but perhaps also for theories of population genetics and evolution.…”

Section: Institute Of Anatomy University Of Zurich Ch-8057 Zurich mentioning

confidence: 99%

A nemesis for heritability estimation

Hirsch¹

1990

Behav Brain Sci

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Mapping genes for manic-depression and schizophrenia with DNA markers

Cited by 10 publications

References 27 publications

Chromosomal Aberrations and Schizophrenia

Chromosomal Aberrations and Schizophrenia

Positive association of dopamine D2 receptor polymorphism with bipolar affective disorder in a European multicenter association study of affective disorders

A nemesis for heritability estimation

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