Source:http://linkedlifedata.com/resource/pubmed/id/12140786
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2002-7-25
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pubmed:abstractText |
Monoamine oxidase A (MAO A) is located on the X chromosome and metabolizes biogenic amines including dopamine, norepinephrine and serotonin. A functional promoter-region polymorphism of this gene has been described that has been studied in a number of mental illnesses but not in attention deficit hyperactivity disorder (ADHD). In the current study, we examined the MAO A promoter-region polymorphism initially in 133 triads and observed preferential transmission of the long alleles from 74 heterozygote mothers to ADHD probands (chi(2) = 4.37, P = 0.036, df = 1). We also examined the role of this polymorphism in a computerized continuous performance test, the TOVA. Significant differences were observed on errors of commission (chi(2) = 7.021, P = 0.008) and patients carrying the long MAO A allele made significantly more such errors. Errors of commission are a measure of impulsivity. However, following Ritalin (methylphenidate) administration the association between this polymorphism and errors of commission was markedly attenuated and no longer significant at the P < 0.05 level. We also analyzed the provisional association by the case-control design. A significant difference in allele frequency was observed between 110 male probands vs 202 male controls (Pearson chi(2) = 7.94, P = 0.047). Similarly results were obtained when 19 female probands were compared to female controls (genotype chi(2) = 21.28; P = 0.0032, 3 df and allele chi(2) = 30.88, P= 0.0007, 2 df). All three complementary approaches employed (family-based, case-control and quantitative trait design) suggest a role for the MAO A promoter-region polymorphism in conferring risk for ADHD in our patient population.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1359-4184
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
7
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
626-32
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12140786-Attention Deficit Disorder with Hyperactivity,
pubmed-meshheading:12140786-Chromosomes, Human, X,
pubmed-meshheading:12140786-DNA,
pubmed-meshheading:12140786-Family,
pubmed-meshheading:12140786-Female,
pubmed-meshheading:12140786-Genotype,
pubmed-meshheading:12140786-Heterozygote Detection,
pubmed-meshheading:12140786-Humans,
pubmed-meshheading:12140786-Male,
pubmed-meshheading:12140786-Monoamine Oxidase,
pubmed-meshheading:12140786-Polymorphism, Genetic,
pubmed-meshheading:12140786-Promoter Regions, Genetic,
pubmed-meshheading:12140786-Psychological Tests,
pubmed-meshheading:12140786-Repetitive Sequences, Nucleic Acid
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pubmed:year |
2002
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pubmed:articleTitle |
Family-based and association studies of monoamine oxidase A and attention deficit hyperactivity disorder (ADHD): preferential transmission of the long promoter-region repeat and its association with impaired performance on a continuous performance test (TOVA).
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pubmed:affiliation |
Geha Mental Health Center, Petak Tikvah, Israel.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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