ADHDgene Database

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Large-scale studies

Data Summary

Published Variant
- SNP: 1391
- CNV: 398
- Others: 173
Published Gene: 359
Published Region: 128
Pathway by PBA: 8
Study: 361

Study Report

Basic Info

Reference	Wang B, 200616389583
Citation	Wang B., Wang Y., Zhou R., Li J., Qian Q., Yang L., Guan L. and Faraone S. V. (2006) "Possible association of the alpha-2A adrenergic receptor gene (ADRA2A) with symptoms of attention-deficit/hyperactivity disorder." Am J Med Genet B Neuropsychiatr Genet, 141B(2): 130-4.
Study Design	family-based
Study Type	Candidate-gene association study
Sample Size	291 ADHD cases and 268 trios
Predominant Ethnicity	Mongoloid
Population	China
Gender	85.8% boys
Age Group	Children/Adolescents : 6-17 years

Detail Info

Summary	The current study first examined the association of the ADRA2A MspI and DraI polymorphisms with ADHD in the Han Chinese population, which differs quite substantially from the Caucasian population in the frequencies of alleles at these polymorphisms. No biased transmission of alleles of either polymorphism was observed using transmission disequilibrium test (TDT) analysis in a sample of 268 nuclear families with an ADHD proband; however, haplotype analysis only identified a trend toward over-transmission of the M/C haplotype to probands with the combined subtype of ADHD. The mm genotype of the MspI polymorphism was also marginally related to lower ADHD symptom scores in a sample of 559 Chinese children with ADHD, which is inconsistent with data from Caucasian samples.
Total Sample	The subjects were recruited from theADHDoutpatient clinic at the Child and Adolescent Psychiatric Division of the Sixth Hospital, Peking University in Beijing, People's Republic of China. For the analyses of transmission disequilibrium, 268 families were included. For the analyses of symptom dimensions, 559 ADHD children were recruited, including the 268 probands from the trios used for transmission disequilibrium analyses.
Sample Collection	Han Chinese
Diagnosis Description	ADHD was diagnosed by DSM-IV criteria through a clinical interview with the subjects and the parents, and it was confirmed in a semistructured interview with the parent (Clinical Diagnostic Interview Scale: CDIS) [Barkley, 1998]. All parents were interviewed with the CDIS by two psychiatrists separately, including one senior psychiatrist. Fifty-four percent of the sample was diagnosed with the inattentive subtype of ADHD (ADHD-I), 39.4% were diagnosed with the combined subtype (ADHD-C), and 6.6% were diagnosed with the hyperactive/impulsive subtype (ADHD-HI).
Technique	DNA was isolated using standard protocols. They genotyped the ADRA2A MspI polymorphism as described by Lario et al. [1997]. In brief, PCR was initiated at 95^oC for 30 sec, 56^oC for 45 sec, and 72^oC for 1 min through 35 cycles. The 20 ul PCR reaction mixture consisted of 0.2 mM dNTP, 2.0 mM MgCl2, X1 Taq reaction buffer (MBI), 1 U Taq polymerase (MBI), and 0.2 uM primers of 5'-TCA CAC CGG AGG TTA CTT CC-3' and 5'-TCCGACGACAGCGCGAGTT-3'. The PCR products were digested with five units of MspI at 37^oC for 4 hr, analyzed on an 8% native polyacrylamide gel, and stained with ethidium bromide. They used the allele terminology (M and m) initially used by Lario et al. [1997]. The DraI polymorphism was amplified using similar PCR conditions with the following primers: 5'-GGA CTA CAA GGG CAT GGC TCA-3' and 5'-TGC TGG TGAAAACGACGACA-3'. The PCR products for this polymorphism were digested with 5 units of DraI, and were detected using 3% agarose gel stained with ethidium bromide.
Analysis Method	For the transmission disequilibrium study, the TDT was performed to explore the possible association of the two ADRA2A polymorphisms with ADHD. They also analyzed possible biased transmission of haplotypes of these two polymorphisms using the TRANSMIT program [version 2.5; Clayton, 1999]. The EH program was utilized to analyze allelic associations [Xie and Ott, 1993]. Groups of probands defined by the genotypes were compared using the nonparametric Kruskal-Wallis H-test and Mann-Whitney U-test due to the non-normal distribution of data. A significance level of 5% was accepted in all comparisons. The statistical tests were conducted using SPSS 11.0 for Windows.
Result Description	No biased transmission of alleles of either polymorphism was observed in a sample of 268 nuclear families, however, haplotype analysis only identified a trend toward over-transmission of the M/C haplotype to probands with the combined subtype of ADHD (X²=3.233,P-value=0.072). The mm genotype of the MspI polymorphism was also marginally related (P-value=0.051) to lower ADHD symptom scores in a sample of 559 Chinese children with ADHD, which is inconsistent with data from Caucasian samples. The results provide weak evidence for a possible role of ADRA2A in ADHD symptom expression.

SNPs reported by this study (count: 2)

SNP	Allele Change	Risk Allele	Statistical Values	Author Comments	Result of Statistical Analysis
rs1800544	M/m		TDT P-value=0.949, McNemar X²=0.004 for ADHD phenotype; TDT P-value=0.213, McNemar X²=1.548 for ADHD-C phenotype; TDT P-value=0.664 for ADHD-HI phenotype; TDT P-value=0.542, McNemar X²=0.371 for ADHD-I phenotype	no biased transmission of any allele was observed no biased transmission of any allele was observed	Non-significant
rs583668	C/T		TDT P-value=0.656, McNemar X²=0.198 for ADHD phenotype; TDT P-value=0.21, McNemar X²=1.568 for ADHD-C phenotype; TDT P-value=0.541 for ADHD-HI phenotype; TDT P-value=0.94, McNemar X²=0.006 for ADHD-I phenotype	no biased transmission of any allele was observed no biased transmission of any allele was observed	Non-significant

Genes reported by this study (count: 1)