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N Craddock

Publications and source records attributed to N Craddock.

120 records · Page 7Linked to original sources
PubMed1993

The dopamine D3 receptor gene: no association with bipolar affective disorder.

Bipolar affective disorder and schizophrenia share many clinical and genetic characteristics, and are thought by some to be different expressions of the same underlying disorder. A recent study showed an excess of homozygosity at a BalI polymorphism in the dopamine D3 receptor gene in schizophrenic patients compared with controls, from two independent centres. We have found no evidence of such an excess in a comparable sample of patients with bipolar affective disorder compared with matched controls. If these findings are confirmed then at least one genetic distinction between these two disorders will have been ascertained and doubt cast upon theories of a common genetic aetiology.

Alleles↗
PubMed1993

Approaches to the genetics of affective disorders.

Affective (mood) disorders are common. There are several methodological impediments to genetic studies of affective disorders, including uncertainties about the best definition of disease phenotype, difficulties in the assessment of lifetime diagnosis and variable age of onset of illness. Despite these difficulties, family, twin and adoption studies provide compelling evidence for the existence of important genetic factors in determining susceptibility to affective disorders. However, the mode of inheritance is unknown. Simple mendelian inheritance may occur in some families but cannot explain the majority of cases. With the advent of polymorphic DNA markers, linkage and association studies have become more useful methods for the genetic analysis of complex disorders such as affective illness. No consistent finding has yet emerged, although chromosomal region 11p15 (and to a lesser extent Xq28) are of continuing interest. In addition to further study of these regions it will also be necessary to look for susceptibility loci in other parts of the genome. Large samples will almost certainly be required. If susceptibility loci of major effect exist then linkage approaches will find them. However, if there are only loci of small effect, then association approaches will be necessary. At present, it seems prudent to pursue both linkage and association approaches together.

Adoption↗
PubMed1993

Linkage is excluded between Darier's disease and the Duffy blood group locus in five British families.

Munro and colleagues (Ann Génét, 1992, 35, 157-160) found small positive lod scores for linkage between the genes for Darier's disease and the Duffy blood locus in two large British families, with a maximum lod score in one family of 0.807 at theta = 0.0. The authors have examined five independent British pedigrees multiply affected by Darier's disease using highly polymorphic microsatellite DNA markers tightly linked to the Duffy locus. They were able to exclude close linkage between the Darier gene and CRP for theta < or = 0.16 and between the Darier gene and D1S104 for theta < or = 0.12. We conclude that the gene for Darier's disease does not lie close to the Duffy locus.

Chromosome Mapping↗
PubMed1991

CPK in NMS.

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Adult↗
PubMedDate not supplied

No evidence for expanded polyglutamine sequences in bipolar disorder and schizophrenia.

Several recent studies have suggested that expanded CAG repeats may contribute to the genetic transmission of bipolar disorder and schizophrenia. In all known disorders associated with expanded CAG repeats, the repeat sequence is translated into glutamine. Therefore the simplest hypothesis is that one or more proteins with expanded polyglutamine sequences are involved in the pathogenesis of bipolar disorder and schizophrenia. In order to examine this hypothesis, we have used an antibody against expanded polyglutamine sequences to examine Western blots prepared from lymphoblastoid cell lines of patients with schizophrenia and bipolar disorder. We also examined Western blots prepared from left frontal cortex tissue samples obtained from 11 schizophrenics post mortem. With the exception of the TATA-binding protein (TBP), we did not detect any proteins containing expanded polyglutamine sequences. Our data therefore suggest either that the expanded repeats which are associated with these disorders do not encode polyglutamine, or that they are within genes that are not expressed within the tissues investigated here.

Adult↗