Study Report
Basic Info
Reference |
Guimaraes AP, 200919756364
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Citation |
Guimaraes A. P., Schmitz M., Polanczyk G. V., Zeni C., Genro J., Roman T., Rohde L. A. and Hutz M. H. (2009) "Further evidence for the association between attention deficit/hyperactivity disorder and the serotonin receptor 1B gene." J Neural Transm, 116(12): 1675-80.
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Study Design |
family-based |
Study Type |
Candidate-gene association study |
Sample Size |
343 families |
Predominant Ethnicity |
Caucasian |
Population |
Brazil |
Gender |
275 (77.9%) males |
Age Group |
Children/Adolescents
:
mean age 10.65 years (SD=3.21)
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Detail Info
Summary |
The aim of this study was to investigate HTR1B gene polymorphisms to determine if there was evidence for biased transmission of haplotypes derived from the 861G>C, -161A>T, and -261T>G from parents to 343 families with ADHD children. They also sought to replicate the findings from Li et al. (2005) and Smoller et al. (2006) that the association between HTR1B is preferentially with ADHD-I. Using a transmission disequilibrium test they found evidence for an excess transmission of haplotype. -261G/-161T/ 861G (P-value=0.014) for affected children in the total sample. When the analysis was repeated with 143 families with ADHD-Inattentive subtype no significant associations were observed. The results provide additional evidence that HRT1B gene may be an important risk factor for the development of ADHD, but this effect seems not to be attributable to inattentive cases. |
Total Sample |
A total of 343 families with an ADHD child were included in the study. The largest sample was composed of 243 children with ADHD clinical diagnosis. The remaining 100 families were of children with ADHD-inattentive type. from the 343 families investigated, 316 (92%) were informative for the family-based association analyses. |
Sample Collection |
Patients were predominantly of European-Brazilian descent (82.1%). The largest sample composed of 243 children with ADHD clinical diagnosis were predominantly of European descent (92.1%). |
Diagnosis Description |
The largest sample was composed of 243 children with ADHD clinical diagnosis recruited at the Child and Adolescent Psychiatric Division of the Hospital de Clinicas de Porto Alegre (HCPA). An ADHD consensus diagnosis based on DSM-IV criteria was achieved as described in detail previously (Roman et al. 2001). The remaining 100 families were of children with ADHD-inattentive type. This group was ascertained from 12 public schools. Inclusion and diagnostic criteria for this sample have been fully described elsewhere (Schmitz et al. 2006). |
Technique |
DNA was extracted from whole blood by a salting out procedure (Lahiri and Nurnberger 1991). The three polymorphisms 861G>C, -161A>T, and -261T>G were genotyped by PCR using primers and methods described elsewhere (Nothen et al. 1994; Lappalainen et al. 1995; Sun et al. 2002). |
Analysis Method |
Pairwise linkage disequilibrium (LD) was estimated using the Multiple Locus Haplotype software (mlocusSNP) (Long 1999). The haplotype family-based association analyses were performed using the statistical program TRANSMIT (Clayton 1999). |
Result Description |
All SNPs investigated were in pairwise significant LD; therefore, all analyses were carried out with haplotypes derived from these three SNPs. Haplotype analyses detected an over-transmission of -261G/-161T/861G haplotype. This haplotype was detected in 30% of the affected subjects. Haplotype -261G/-161T/861C which occurred in a low frequency was under-transmitted. However, when the same analyses were carried out only with 143 families with ADHD-I subtype no preferential transmission of alleles from parents to probands was observed. No association was observed between the HTR1B gene haplotypes and ADHD with any specific comorbid condition. |
Genes reported by this study (count: 1)
Gene |
Statistical Values/Author Comments |
Result of Statistical Analysis |
HTR1B |
haplotype analyses: P-value=0.014. detected an over-transmis......
haplotype analyses: P-value=0.014. detected an over-transmission of -261G/-161T/861G haplotype in this gene.
More...
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Significant
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