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| Research article summary (published 3 Sep 2006): |
MAOA promoter polymorphism and attention deficit hyperactivity disorder (ADHD) in indian children.
Full Abstract
Attention deficit hyperactivity disorder (ADHD) is a highly disabling, early onset childhood neurobehavioral disorder with a higher occurrence in boys as compared to girls. Pharmacological and molecular genetic studies have revealed the influence of dopaminergic and serotonergic systems in the etiology of the disorder. Monoamine oxidase A (MAOA) is a mitochondrial enzyme that regulates the dopaminergic signals in the pre-synaptic region. Polymorphism in the promoter region of the MAOA gene, which comprises of 30 bp repeats with repeat number varying between 2.5, 3.5, 4.5, and 5.5, has been shown to be associated with various neurobehavioral disorders including ADHD. This is the first study on Indian ADHD cases to validate an association between transmission of MAOA promoter polymorphism and risk of ADHD. We have analyzed the MAOA promoter polymorphism in a group of ADHD probands, their parents and ethnically matched controls by UNPHASED. Our findings indicate significant difference in the frequency of 3.5 repeat allele (P = 0.02) between cases and controls and preferential transmission of the short allele (3.5 repeat) from mothers to male ADHD probands (P = 0.005). We conclude that the short 3.5 repeat allele of the MAOA-u VNTR is probably associated with ADHD in our population and could be the reason for making boys prone to ADHD as compared to girls.
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Author information
Author/s: Das, Manali (M); Bhowmik, Aneek Das (AD); Sinha, Swagata (S); Chattopadhyay, Anindita (A); Chaudhuri, Keya (K); Singh, Manoranjan (M); Mukhopadhyay, Kanchan (K);
Affiliation: Manovikas Biomedical Research and Diagnostic Centre, E.M. Bypass, Kolkata, India.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics (Am J Med Genet B Neuropsychiatr Genet), published in United States. (Language: eng)
Reference: 2006-Sep; vol 141B (issue 6) : pp 637-42
Dates: Created 2006/08/30; Completed 2006/10/18; Revised 2008/11/21;
PMID: 16856146, status: MEDLINE (last retrieval date: 12/26/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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