| Summary |
In this study, they tested the gene for linkage to ADHD by genotyping two polymorphisms in the MOG gene-a dinucleotide repeat located upstream from the MOG transcription start site and a Val145Ile substitution in exon 3-in a sample of 104 nuclear families identified through a proband with ADHD. They examined the transmission of the alleles of the Val145Ile and the dinucleotide repeat polymorphisms using the transmission disequilibrium test. They did not observe biased transmission of the alleles at either polymorphism to ADHD probands or siblings. Their findings using this sample do not support the role of the MOG gene in ADHD. |
| Total Sample |
In total, 104 nuclear families were genotyped for this study, 79 with a proband with both parental DNAs genotyped and 25 with a proband and with DNA available and genotyped for a single parent. Twenty-one siblings of the probands who also meet our criteria for ADHD were included in the analysis. |
| Sample Collection |
The assessment and characteristics of the subjects for this study have been previously described [Barr et al., 1999, 2000a, 2000b, 2000c]. |
| Diagnosis Description |
Briefly, subjects were included if they met DSM-IV criteria for ADHD. Information used for the diagnosis of ADHD and comorbid conditions was obtained from a semi-structured interview for parents (Parent Interview for Child Symptoms, PICS-IV; data not shown) and teachers (Teacher Telephone Interview-IV, TTI; data not shown), supplemented with the following questionnaires and child assessment instruments: Conners Parent and Teacher Rating Scales, Revised [Conners, 1997], the Ontario Child Health Survey Scales, Revised [Boyle et al., 1993], Clinical Evaluation of Language Fundamentals, 3rd edition [Semel et al., 1995], Children's Depression Inventory [Kovacs, 1995], and Children's Manifest Anxiety Scale [Reynolds and Richmond, 1985]. Of the subjects that were used in this study, 57% of the children were of the combined subtype, 19% were of the hyperactive/impulsive subtype, and 24% were of the primarily inattentive subtype. |
| Technique |
DNA was extracted directly from blood lymphocytes using a high salt extraction method [Miller et al., 1988]. A 171 bp fragment of exon 3 was amplified to genotype the Val145Ile substitution [Rodriguez et al., 1997]. They used 100 ng of each of the primers MOGEX3.A (5'-CAAATGTCAGTCCT-3') and MOGEX3.B (5'-TCCACCCACCCTC-3'), 0.2 mM dNTP, 1.5 mM magnesium chloride, and 0.5 U Taq polymerase in a 20ul total reaction volume. The 5' dinucleotide repeat, located upstream from the MOG transcription start site, was genotyped using the primers MOG 31 (5'-GAAATGTGAGAATAAAGGAGA) and MOG 32 (5'-GATAAAGGGGAACTACTACA) [Roth et al., 1995]. The primer MOG 31 was labeled with the fluorescent dye HEX. |
| Analysis Method |
The TDT statistic was calculated using the extended TDT (ETDT) program [Sham and Curtis, 1995]. |
| Result Description |
They did not observe biased transmission of the alleles at either polymorphism to ADHD probands or siblings. Their findings using this sample do not support the role of the MOG gene in ADHD. |
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