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    MITOCHONDRIAL DNA COPY NUMBER IS ASSOCIATED WITH ATTENTION DEFICIT HYPERACTIVITY DISORDER

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    Background: Attention deficit hyperactivity disorder (ADHD) is the most common psychiatric disorder in children. Several hypotheses have been proposed to explain its etiology. Mitochondrial dysfunction (MD) is suggested to be one of the causes of Attention Deficit Hyperactivity Disorder. The objective of the study was to evaluate the relationship between MD and ADHD by investigating mitochondrial DNA (mtDNA) levels from peripheral blood leukocytes, one of the best biomarkers of mitochondrial dysfunction. Subjects and methods: This study included 56 children aged 6-16 years who were diagnosed with ADHD for the first time and 56 age- and sex matched children without ADHD. Real-time PCR was performed to determine the relative mtDNA copy number in each study participant. Results: The mean mtDNA copy number of the case group was 57.623±24.827 and that of the control group was 44.204±18.926 (p=0.002). The mtDNA copy number of the case group was higher than that of the control group. Results of ROC curve analysis provided a mtDNA cutoff value of 45. Conclusion: Significantly higher mtDNA copy number in ADHD group may suggest mitochondrial dysfunction in the etiopathogenesis of ADHD

    MITOCHONDRIAL DNA COPY NUMBER IS ASSOCIATED WITH ATTENTION DEFICIT HYPERACTIVITY DISORDER

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    Background: Attention deficit hyperactivity disorder (ADHD) is the most common psychiatric disorder in children. Several hypotheses have been proposed to explain its etiology. Mitochondrial dysfunction (MD) is suggested to be one of the causes of Attention Deficit Hyperactivity Disorder. The objective of the study was to evaluate the relationship between MD and ADHD by investigating mitochondrial DNA (mtDNA) levels from peripheral blood leukocytes, one of the best biomarkers of mitochondrial dysfunction. Subjects and methods: This study included 56 children aged 6-16 years who were diagnosed with ADHD for the first time and 56 age- and sex-matched children without ADHD. Real-time PCR was performed to determine the relative mtDNA copy number in each study participant. Results: The mean mtDNA copy number of the case group was 57.623±24.827 and that of the control group was 44.204±18.926 (p=0.002). The mtDNA copy number of the case group was higher than that of the control group. Results of ROC curve analysis provided a mtDNA cutoff value of 45. Conclusion: Significantly higher mtDNA copy number in ADHD group may suggest mitochondrial dysfunction in the etiopathogenesis of ADHD
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