Study Report
Basic Info
Reference |
Faraone SV, 200818081027
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Citation |
Faraone S. V., Doyle A. E., Lasky-Su J., Sklar P. B., D'Angelo E., Gonzalez-Heydrich J., Kratochvil C., Mick E., Klein K., Rezac A. J. and Biederman J. (2008) "Linkage analysis of attention deficit hyperactivity disorder." Am J Med Genet B Neuropsychiatr Genet, 147B(8): 1387-91.
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Study Design |
affected sib pairs |
Study Type |
Genome-wide linkage study |
Sample Size |
271 families, 1170 individuals |
Predominant Ethnicity |
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Population |
USA |
Gender |
358 males and 243 females in analysis 1; 577 males and 523 females in analysis 2 |
Age Group |
Children/Adolescents
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Detail Info
Summary |
They genotyped 5,980 SNPs across the genome in 1,187 individuals from families with children diagnosed with ADHD. They then performed two nonparametric linkage analyses on ADHD families: (1) an affected sibling pair linkage analysis on 217 families with 601 siblings diagnosed with ADHD and (2) a variance components linkage analysis using the number of ADHD symptoms as the phenotype on 260 families with 1,100 phenotyped siblings. The affection status linkage analysis had a maximum LOD score of 1.85 on chromosome 8 at 54.2 cM. The maximum LOD score in the variance components linkage analysis was 0.8 on chromosome 8 at 93.4 cM. The absence of regions of significant or suggestive linkage in these data suggest that there are no genes of large effect contributing to the ADHD phenotype. |
Total Sample |
an affected sibling pair linkage analysis on 217 families with 601 siblings diagnosed with ADHD and a variance components linkage analysis using the number of ADHD symptoms as the phenotype on 260 families with 1,100 phenotyped siblings. |
Diagnosis Description |
A two-stage procedure selected the final sample. The first stage confirmed the diagnosis of the sibling pair with the primary caregiver or adult sibling pair using a telephone questionnaire that included ADHD and exclusion criteria. The second stage was a structured interview (details in the original publication). Families with sibling pairs receiving positive diagnoses at both stages were included in the study. |
Technique |
Genotyping services were provided by the Center for Inherited Disease Research (CIDR) using 5,980 single nucleotide polymorphisms (SNPs) spaced at an average of ~121 kb intervals, following CIDR's standard genotyping procedures. In brief, CIDR performs whole genome SNP linkage scan genotyping using Illumina's BeadArrayTM technology on a BeadLab system. CIDR uses the Illumina1 Linkage IVb Marker Panel. Using this Illumina platform a total of 6,008 total SNP assays were attempted for genotyping. |
Analysis Method |
Two multipoint nonparametric genetic linkage analyses were preformed on these data. Empirical simulation to establish genomewide significance were performed if aLODscore greater than 3.0 was achieved in either linkage analysis. Such simulations were performed in MERLIN[Abecasis et al., 2002]. |
Result Description |
The affection status linkage analysis had a maximum LOD score of 1.85 on chromosome 8 at 54.2 cM. The maximum LOD score in the variance components linkage analysis was 0.8 on chromosome 8 at 93.4 cM. |
Regions reported by this study (count: 3)
Region |
Statistical Values |
Author Comments |
Result of Statistical Analysis |
Chr8:54.2cM |
LOD score=1.85 |
no convincing evidence for linkage
no convincing evidence for linkage
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Non-significant
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Chr15:51.7cM |
LOD score=1.81 |
no convincing evidence for linkage
no convincing evidence for linkage
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Non-significant
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Chr8:93.4cM |
LOD score=0.8 |
no convincing evidence for linkage
no convincing evidence for linkage
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Non-significant
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