Systematic and detailed chromosome analysis, combined with a semistructured interview, was performed in 2 families with schizophrenia and in 2 families with manic depressive illness. Prometaphase technique did not reveal any subtle structural chromosome abnormalities. However, in standard techniques
Linkage study between manic-depressive illness and chromosome 21
โ Scribed by Ewald, Henrik; Eiberg, Hans; Mors, Ole; Flint, Tracey; Kruse, Torben A.
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 79 KB
- Volume
- 67
- Category
- Article
- ISSN
- 0148-7299
- DOI
- 10.1002/(sici)1096-8628(19960409)67:2<218::aid-ajmg15>3.0.co;2-m
No coin nor oath required. For personal study only.
โฆ Synopsis
Chromosome 21, of interest as potentially containing a disease gene for manic-depressive illness as possible evidence for a gene predisposing to affective disorder, has recently been reported in a single large family as well as samples of families.
The present study investigates for linkage between manic-depressive illness and markers covering the long arm of chromosome 21 in two manic-depressive families, using ten microsatellite polymorphisms as markers.
No conclusive evidence for a disease gene on the long arm of chromosome 21 was found. Assuming either a dominant or recessive mode of inheritance, close linkage to the marker PFKL, which has been reported as possibly linked to affective disorder, seems unlikely in the families studied here. PFKL and more telomeric markers yielded small positive lod scores at higher recombination fractions in the largest family, and small positive lod scores at lower recombination fractions in the affecteds-only analyses in the smallest family.
๐ SIMILAR VOLUMES
Over the last three years several studies have investigated the hypothesis of linkage between bipolar disorder and markers on chromosome 18. Although independent groups have reported positive results, it is still not clear how these should be interpreted, as linkage spans a considerably large segmen
Evidence consistent with the existence of genetic linkage between bipolar disorder and three regions on chromosome 18, the pericentromeric region, 18q21, and 18q22-q23 have been reported. Some analyses indicated greater evidence for linkage in pedigrees in which paternal transmission of disease occu
The report of the 1997 workshop presented overall evidence providing strong support for a susceptibility locus for bipolar disorder at C21q22-23. The 1998 workshop considered the latest results from four groups, and additional studies also have been incorporated into this report. The workshop noted
## There have been several conflicting reports of association of monoamine oxidase (MAO) A gene polymorphisms and bipolar affective disorder. In order to determine the possible role of the MAO region in susceptibility to affective disorders in an independent sample, we have genotyped 83 probands o
Genetic epidemiology has provided consistent evidence over many years that schizophrenia has a genetic component, and that this genetic component is complex, polygenic, and involves epistatic interaction between loci. Molecular genetics studies have, however, so far failed to identify any DNA varian