Study Report

Basic Info
| Reference |
Turecki, G.,2000 PMID: 10760559
|
| Citation |
Turecki, G., M. Alda, et al. (2000). "Polyglutamine coding genes in bipolar disorder: lack of association with selected candidate loci." J Affect Disord 58(1): 63-68.
|
| Disease Type |
Bipolar Disorder |
| Study Design |
case-control |
| Study Type |
Candidate-gene association study |
| Sample Size |
138 cases and 108 controls |
| SNP/Region/Marker Size |
5 variants |
| Predominant Ethnicity |
Caucasian |
| Population |
Austrian, Canadian,Czech, Danish, German, and Swedish |
| Gender |
The sex ratio(M/F) was 0.87 for BD patients and 0.86 for controls |
| Age Group |
Adults
:
Mean age(SD)(year):50.0(14.4),27.6(9.9) at onset for BD patients and 51.5(14.8) for controls
|

Detail Info
| Sample Diagnosis |
RDC |
| Sample Status |
Subjects included in this study were 138 patients and 108 screened normal controls that were collected in centers that collaborate in the International Group for the Study of Lithium (IGSLi). Research clinics in Austria, Germany, Denmark, Sweden, Czech Republic and Canada contributed 3, 23, 7, 17, 20 and 68 patients, respectively. Controls were married-insubjects from a family study of this patient population or healthy volunteers of the same ethnic background as cases. All patients and controls were Caucasians of European (non-Mediterranean) descent. |
| Technique |
PCR and sequencing |
| Statistical Method |
Alleles and genotype distributions were compared between groups using the method respecproposed by Curtis and Sham that estimates empirical P values using a Monte Carlo approach (Sham and Curtis, 1995). |
| Result Summary |
No difference was found in allele distribution between cases and controls for any of the loci studied. In one locus - L10378 - patients had a tendency to present shorter alleles (28.1 versus 27.9 repeats; t=2.55, df=205, P=0.011), however, this difference disappeared after correction for multiple testing. LIMITATIONS: The study has limitations common to most candidate gene association studies, that is, limited number of loci investigated and limited power to detect loci that account for a small proportion of the total genetic variability. Our results suggest that the loci investigated have no major role in the genetic predisposition to bipolar disorder. |

Other variants reported by this study for BD (count: 1)
| Variant Name |
Related Gene |
Type |
Allele Change |
Risk Allele |
Statistical Values |
Author Comments |
Result Category |
| TBP CAG/CAA repeats |
TBP |
microsatellite |
CAG/CAA repeats |
|
Association analysis:Monte Carlo approach, P-value > 0.05
|
No significant association was observed in BD.
No significant association was observed in BD.
|
Negative
|

Genes reported by this study for BD (count: 1)
| Gene |
Statistical Values/Author Comments |
Result Category |
| TBP |
No significant association was observed in BD.
No significant association was observed in BD.
|
Negative
|

Regions reported by this study for BD (count: 4)
| Region |
Statistical Values |
Author Comments |
Result Category |
| 16q13 |
Association analysis: Monte Carlo approach, t = 2.55, df = 205, P-value = 0.011(P-value > 0.05 after correction)
|
No significant association was observed in BD.
No significant association was observed in BD.
|
Negative
|
| 2q32.3-q33 |
Association analysis: Monte Carlo approach, P-value > 0.05
|
No significant association was observed in BD.
No significant association was observed in BD.
|
Negative
|
| 22q11.2 |
Association analysis: Monte Carlo approach, P-value > 0.05
|
No significant association was observed in BD.
No significant association was observed in BD.
|
Negative
|
| Chr 17 |
Association analysis: Monte Carlo approach, P-value > 0.05
|
No significant association was observed in BD.
No significant association was observed in BD.
|
Negative
|