سامانه مدیریت نشریات علمی دانشگاه علوم پزشکی مشهد

Mehdizadeh Fanid, Leila, Tayefeh_gholami, Samaneh, Akbarzadeh, Sama, Valatabar, Nazila, HosseinpourFeizi, MohammadAli. (1401). The rs6323 and uVNTR Polymorphisms in the MAOA Gene are Associated with Attention Deficit Hyperactivity Disorder in Iranian Azeri Children. , 10(9), 16712-16718. doi: 10.22038/ijp.2022.65546.4938
Leila Mehdizadeh Fanid; Samaneh Tayefeh_gholami; Sama Akbarzadeh; Nazila Valatabar; MohammadAli HosseinpourFeizi. "The rs6323 and uVNTR Polymorphisms in the MAOA Gene are Associated with Attention Deficit Hyperactivity Disorder in Iranian Azeri Children". , 10, 9, 1401, 16712-16718. doi: 10.22038/ijp.2022.65546.4938
Mehdizadeh Fanid, Leila, Tayefeh_gholami, Samaneh, Akbarzadeh, Sama, Valatabar, Nazila, HosseinpourFeizi, MohammadAli. (1401). 'The rs6323 and uVNTR Polymorphisms in the MAOA Gene are Associated with Attention Deficit Hyperactivity Disorder in Iranian Azeri Children', , 10(9), pp. 16712-16718. doi: 10.22038/ijp.2022.65546.4938
Mehdizadeh Fanid, Leila, Tayefeh_gholami, Samaneh, Akbarzadeh, Sama, Valatabar, Nazila, HosseinpourFeizi, MohammadAli. The rs6323 and uVNTR Polymorphisms in the MAOA Gene are Associated with Attention Deficit Hyperactivity Disorder in Iranian Azeri Children. , 1401; 10(9): 16712-16718. doi: 10.22038/ijp.2022.65546.4938

The rs6323 and uVNTR Polymorphisms in the MAOA Gene are Associated with Attention Deficit Hyperactivity Disorder in Iranian Azeri Children

Journal of Pediatric Perspectives
مقاله 11، دوره 10، شماره 9، آذر 2022، صفحه 16712-16718    اصل مقاله (419.83 K)
نوع مقاله: original article
شناسه دیجیتال (DOI): 10.22038/ijp.2022.65546.4938
نویسندگان
Leila Mehdizadeh Fanid* 1؛ Samaneh Tayefeh_gholami2؛ Sama Akbarzadeh3؛ Nazila Valatabar4؛ MohammadAli HosseinpourFeizi4
1Department of Cognitive Neuroscience, Faculty of Education and Psychology University of Tabriz, Tabriz, Iran.
2Department of Animal biology, Faculty of Natural Sciences, University of Tabriz
3Animal biology, Natural sciences, University of Tabriz, Tabriz, Iran
4Department of Animal Biology¸ Faculty of Natural Sciences¸ University of Tabriz
چکیده
Background: ADHD is the most prevalent psychiatric health issue in youth, which may also affect adults. Environmental and genetic factors both contribute significantly to the development and progression of this condition. Monoamine oxidases, which catalyze the metabolism of dopaminergic neurotransmitters, are involved in the pathogenesis of ADHD. The purpose of this study was to determine the connection between polymorphic variations rs6323 and uVNTR in the (Un translate variable nucleotide tandem repeat) MAO-A gene and the risk for ADHD in Iranian-Azeri children.
Methods: Clinical evaluation was used to recruit 137 ADHD patients (female 22, male 115) and 100 controls (female 48, male 52) from the East Azerbaijan region in northern Iran. Genomic DNA was taken from their peripheral blood samples and genotyping was performed using PCR-based amplification of target sites. SPSS (Version 16) and the javastat online statistics program (http://statpages.org/ctab2x2.html) were used for statistical analysis.
Results: The rs6323TT genotype was shown to be a significant risk factor for ADHD (OR 3.619, 95 percent CI 0.878-17.213, p = 0.044). In comparison, no significant differences in allele frequencies were observed between ADHD patients and the control group (p > 0.05). The 5R allele of uVNTR was shown to have a substantial protective impact against the development of ADHD (OR0.349, 95 percent confidence interval 0.151-0.797, p = 0.006).
Conclusion: Our findings indicate that MAOA gene polymorphisms may play a role in the start and development of ADHD in Iranian-Azeri youngsters. However, more research with larger sample sizes is necessary to corroborate these results.
کلیدواژه‌ها
ADHD؛ MAOA؛ polymorphism؛ Iranian-Azeri children
مراجع
  1. Tsai M-C, Jhang K-J, Lee C-T, Lin Y-F, Strong C, Lin Y-C, Strong C, Lin YC, Hsieh YP, Lin CY. Effects of Childhood Adversity and Its Interaction with the MAOA, BDNF, and COMT Polymorphisms on Subclinical Attention Deficit/Hyperactivity Symptoms in Generally Healthy Youth. Children. 2020; 7(9):122.
  2. Sayal K, Prasad V, Daley D, Ford T, Coghill D. ADHD in children and young people: prevalence, care pathways, and service provision. The Lancet Psychiatry. 2018; 5(2):175-86.
  3. Amiri S, Malek A, Sadeghi-Bazargani H, Mansouri M, Fanid LM, Abdi S, et al. Screening of attention deficit hyperactivity disorder in children aged 3 to 6 years and 11 month olds of Tabriz, North-West of Iran. Australasian Medical Journal. 2018; 11(11).
  4. Hwang IW, Lim MH, Kwon HJ, Jin HJ. Association of Monoamine Oxidase A (MAOA) gene uVNTR and rs6323 polymorphisms with attention deficit and hyperactivity disorder in Korean children. Medicina. 2018; 54(3):32.
  5. Mehdizadeh Fanid L, Adampurzare M, HosseinpourFeizi MA. The Association of DRD2 Gene TaqI Polymorphism with Attention Deficit Hyperactivity Disorder a Population Sample of Iranian Azeri-children. International Journal of Pediatrics. 2016; 4(5):1803-7.
  6. Faraone SV, Mick E. Molecular genetics of attention deficit hyperactivity disorder. Psychiatric Clinics. 2010; 33(1):159-80.
  7. Oh S-Y, Kim Y-K. Association of norepinephrine transporter gene polymorphisms in attention-deficit/hyperactivity disorder in the Korean population. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2017; 73:56-63.
  8. Xu MK, Gaysina D, Tsonaka R, Morin AJ, Croudace TJ, Barnett JH, Houwing-Duistermaat J, Richards M, Jones PB, the LHA Genetics Group. Monoamine oxidase A (MAOA) gene and personality traits from late adolescence through early adulthood: A latent variable investigation. Frontiers in Psychology. 2017; 8:1736.
  9. Kõks G, Prans E, Ho XD, Duy BH, Tran HD, Ngo NB, Hoang LN, Tran HM, Bubb VJ, Quinn JP, Kõks S. Genetic interaction between two VNTRs in the MAOA gene is associated with the nicotine dependence. Experimental Biology and Medicine. 2020; 245(8):733-9.
  10. Pueyo N, Navarro J, Fatjó-Vilas M, de la Osa N, Penelo E, Fañanás L, Ezpeleta L. Monoamine oxidase A (MAOA) interaction with parenting practices on callous-unemotional traits in preschoolers. The European Journal of Psychiatry. 2021; 35(4):225-33.
  11. Wei Y-L, Li C-X, Li S-B, Liu Y, Hu L. Association study of monoamine oxidase A/B genes and schizophrenia in Han Chinese. Behavioral and Brain Functions. 2011; 7(1):1-6.
  12. Liu Z, Huang L, Luo X-j, Wu L, Li M. MAOA variants and genetic susceptibility to major psychiatric disorders. Molecular neurobiology. 2016; 53(7):4319-27.
  13. Das M, Das Bhowmik A, Sinha S, Chattopadhyay A, Chaudhuri K, Singh M, Mukhopadhyay K. MAOA promoter polymorphism and attention deficit hyperactivity disorder (ADHD) in Indian children. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 2006; 141(6):637-42.
  14. Ducci F, Newman T, Funt S, Brown G, Virkkunen M, Goldman D. A functional polymorphism in the MAOA gene promoter (MAOA-LPR) predicts central dopamine function and body mass index. Molecular Psychiatry. 2006; 11(9):858-66.
  15. Manca M, Pessoa V, Lopez AI, Harrison PT, Miyajima F, Sharp H, Pickles A, Hill J, Murgatroyd C, Bubb VJ, Quinn JP. The regulation of monoamine oxidase, a gene expression by distinct variable number tandem repeats. Journal of Molecular Neuroscience. 2018; 64(3):459-70.
  16. Pickles A, Hill J, Breen G, Quinn J, Abbott K, Jones H, Sharp H. Evidence for interplay between genes and parenting on infant temperament in the first year of life: monoamine oxidase A polymorphism moderates effects of maternal sensitivity on infant anger proneness. Journal of child psychology and psychiatry. 2013; 54(12):1308-17.
  17. Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, Müller U, Aguet M, Babinet C, Shih JC, Maeyer ED. Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. Science. 1995; 268(5218):1763-6.
  18. Crockett MJ, Clark L, Hauser MD, Robbins TW. Serotonin selectively influences moral judgment and behavior through effects on harm aversion. Proceedings of the National Academy of Sciences. 2010; 107(40):17433-8.
  19. Kim-Cohen J, Caspi A, Taylor A, Williams B, Newcombe R, Craig IW, Moffitt TE. MAOA, maltreatment, and gene–environment interaction predicting children's mental health: new evidence and a meta-analysis. Molecular psychiatry. 2006; 11(10):903-13.
  20. Buckholtz JW, Meyer-Lindenberg A. MAOA and the neurogenetic architecture of human aggression. Trends in neurosciences. 2008; 31(3):120-9.
  21. Rodriguez S, Gaunt TR, Day IN. Hardy-Weinberg equilibrium testing of biological ascertainment for Mendelian randomization studies. American journal of epidemiology. 2009; 169(4):505-14.
  22. Karmakar A, Goswami R, Saha T, Maitra S, Roychowdhury A, Panda CK, Sinha S, Ray A, Mohanakumar KP, Rajamma U, Mukhopadhyay K. Pilot study indicates role of preferentially transmitted monoamine oxidase gene variants in behavioral problems of male ADHD probands. BMC medical genetics. 2017; 18(1):1-12.
  23. Salem AM, Ismail S, Zarouk WA, Abdul Baky O, Sayed AA, El-Hamid A, Salem S. Genetic variants of neurotransmitter-related genes and miRNAs in Egyptian autistic patients. The Scientific World Journal. 2013; 2013.
  24. Wu Y-H, Fischer DF, Swaab DF. A promoter polymorphism in the monoamine oxidase A gene is associated with the pineal MAOA activity in Alzheimer's disease patients. Brain research. 2007; 1167:13-9.
  25. Brummett BH, Krystal AD, Siegler IC, Kuhn C, Surwit RS, Züchner S, et al. Associations of a regulatory polymorphism of monoamine oxidase-A gene promoter (MAOA-uVNTR) with symptoms of depression and sleep quality. Psychosomatic medicine. 2007; 69(5):396.
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