No evidence of association from transmission disequilibrium analysis of the hKCa3 gene in bipolar disorder

Bipolar Disord. 2000 Dec;2(4):328-31. doi: 10.1034/j.1399-5618.2000.020406.x.

Abstract

Objective: A recent case control study has suggested that modest enlargements of a highly polymorphic CAG repeat in exon 1 of the gene encoding potassium channel hKCa3 may be associated with bipolar disorder (BPD). We have examined this hypothesis by genotyping this locus in a family-based association study.

Method: One hundred and twenty-eight parent offspring trios of British Caucasian origin were examined where the proband was diagnosed with the American Psychiatric Association's Diagnostic and Statistical Manual (DSM)-IV BPD I (n = 123) or II (n = 5). An improved assay was used, with redesigned polymerase chain reaction (PCR) primers, permitting quicker and higher resolution genotyping. The resultant genotypes were analysed using the extended transmission/ disequilibrium test (ETDT).

Results: The experimental data did not provide evidence for the preferential transmission of large alleles to bipolar cases (chi2 = 11.12, df = 10, p = 0.349).

Conclusions: Our data provide no support for the hypothesis that variation at the hKCa3 gene contributes to susceptibility to BPD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Alleles
  • Bipolar Disorder / genetics*
  • Chi-Square Distribution
  • Female
  • Genotype
  • Humans
  • Linkage Disequilibrium / genetics*
  • Male
  • Middle Aged
  • Parents*
  • Polymorphism, Genetic
  • Potassium Channels / genetics*
  • Potassium Channels, Calcium-Activated*
  • Small-Conductance Calcium-Activated Potassium Channels
  • Trinucleotide Repeat Expansion / genetics*

Substances

  • KCNN3 protein, human
  • Potassium Channels
  • Potassium Channels, Calcium-Activated
  • Small-Conductance Calcium-Activated Potassium Channels