HLA System and Affective Disorders: A Sibship Genetic Study

Smeraldi, Enrico; Negri, F.; Melica, A. M.; Scorza-Smeraldi, R.

doi:10.1111/j.1399-0039.1978.tb01334.x

Cited by 38 publications

(4 citation statements)

References 11 publications

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“…Results of this analysis suggested linkage. A sib pair analysis of these data pooled with data from Weitkamp et al (1980, in which bipolar individuals were not included), Targum et al (1979), and Smeraldi (Smeraldi & Bellodi, 1981;Smeraldi et al, 1978) also suggested linkage. More specifically, an analysis of sibships having only two affected members indicated linkage, whereas the analysis of sibships having three or more ill members did not find evidence of linkage.…”

Section: Hla Linkagementioning

confidence: 94%

“…The affected sib pair method does not allow simple estimation of the recombination fraction, but it does not require assumptions about the mode of inheritance. Smeraldi and colleagues (Smeraldi & Bellodi, 1981; Smeraldi, Negri, Melica, & Scorza-Smeraldi, 1978) examined HLA linkage to affective disorders in 26 families by means of the sib pair method. Illness was defined by RDC for bipolar or unipolar disorders.…”

Section: Linkage Analysesmentioning

confidence: 99%

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Genetic transmission of major affective disorders: Quantitative models and linkage analyses.

Faraone¹,

Kremen²,

Tsuang³

1990

Psychological Bulletin

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We comprehensively reviewed 2 types of studies aimed at specifying the mode of inheritance of major affective disorders: quantitative models and linkage analyses. Quantitative models attempt to represent the genetic mechanism responsible for the familial distribution of a disorder. Despite efforts to refine models by incorporating the bipolar-unipolar distinction or the sex effect, consistent support for a specific mode of transmission has not been found. Some mixed genetic models support single major locus inheritance, but transmission probabilities do not conform to Mendelian expectations. Linkage analysis is a more powerful technique used for testing the single gene hypothesis. Linkage results have also been inconsistent, showing moderate support for an X-linked variant of bipolar-related disorder and equivocal support for linkages to Chromosomes 6 and 11. However, relatively few genetic loci have been examined. Methodological factors, genetic heterogeneity, and phenotypic heterogeneity are discussed as potential explanations for inconsistent findings.

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Section: Hla Linkagementioning

confidence: 94%

Section: Linkage Analysesmentioning

confidence: 99%

Genetic transmission of major affective disorders: Quantitative models and linkage analyses.

Faraone¹,

Kremen²,

Tsuang³

1990

Psychological Bulletin

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“…Several such studies have been attempted in MDI, but no conclusive evidence for linkage has been found. With the HLA system, both linkage and association have been reported (Smeraldi et al 1978, Weitkamp et al 1981, Weitkamp & Stancer 1989, Stancer et al 1988. However, a review of 18 such studies did not support the earlier findings (Tsuang & Faraone 1990).…”

mentioning

confidence: 93%

Suggestion of linkage between manic‐depressive illness and the enzyme phosphoglycolate phosphatase (PGP) on chromosome 16p

Eiberg¹,

Ewald²,

Mors³

1993

Clinical Genetics

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Eiberg H, Ewald H, Mors O. Suggestion of linkage between manic‐depressive illness and the enzyme phosphoglycolate phosphatase (PGP) on chromosome 16p. Clin Genet 1993: 44: 254–257. © Munksgaard, 1993 Two large Danish pedigrees with manic‐depressive illness (MDI) were ascertained through bipolar probands. The pedigrees include bipolar as well as unipolar cases. An autosomal dominant mode of inheritance with incomplete penetrance was assumed. Linkage relationships between MDI and 37 autosomal serum, enzyme and blood group markers were investigated. For phosphoglycolate phosphatase, a maximum lod score of 2.20 at 0% recombination was found for the largest family. The other family was not informative. This may suggest assignment of a major gene for MDI to chromosome 16p13.

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“…Following Green and Woodrow's advice, a large number of investigators apparently only consider for analysis families in which all four parental haplotypes can be identified with certainty (see, for instance, Smeraldi et al 1978). This practice is wasteful since ambiguous sibships contain considerable information.…”

mentioning

confidence: 99%

The distribution of HLA haplotypes in families with one untyped parent

Suarez

Rice

1982

Tissue Antigens

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For non‐Mendelian diseases, the distribution of shared haplotypes in multiplex sibships provides a powerful tool to investigate the hypothesis that disease susceptibility genes map in the neighborhood of the HLA complex. Occasionally, ambiguous sibships arise because all offspring inherit an HLA haplotype that is identical in state from an untyped parent. The scoring procedure developed here uses the population frequency of the haplotype as well as the sibship size to estimate the probability that, with respect to the untyped parent, all sibs are identical by descent. The resulting score from an ambiguous sibship can then be combined with scores from unambiguous sibships to form the statistic suggested by Green & Woodrow. It is shown that failure to include this type of ambiguous sibship may result in a significant loss of information.

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HLA System and Affective Disorders: A Sibship Genetic Study

Cited by 38 publications

References 11 publications

Genetic transmission of major affective disorders: Quantitative models and linkage analyses.

Genetic transmission of major affective disorders: Quantitative models and linkage analyses.

Suggestion of linkage between manic‐depressive illness and the enzyme phosphoglycolate phosphatase (PGP) on chromosome 16p

The distribution of HLA haplotypes in families with one untyped parent

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