Volume 9, Issue 6 (November & December 2018)                   BCN 2018, 9(6): 429-438 | Back to browse issues page


XML Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Ahmadi L, Kazemi Nezhad S R, Behbahani P, Khajeddin N, Pourmehdi-Boroujeni M. Genetic Variations of DAOA (rs947267 and rs3918342) and COMT Genes (rs165599 and rs4680) in Schizophrenia and Bipolar I Disorder. BCN. 2018; 9 (6) :429-438
URL: http://bcn.iums.ac.ir/article-1-908-en.html
1- Department of Genetics, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
2- Department of Psychiatry, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
3- Department of Food Hygiene, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Abstract:  
Introduction: Genetic and environmental factors are involved in the incidence of schizophrenia and bipolar disorder. Many reports confirm that several common genes are connected with these two psychotic disorders. Several neurotransmitters may be involved in the molecular mechanisms of schizophrenia and bipolar disorder. We aimed to estimate the role of two talent genes: DAOA in neurotransmission of glutamate and COMT in neurotransmission of dopamine to guide the treatment of schizophrenia and bipolar disorder. 
Methods: Blood samples (n=100 for schizophrenia, n=100 for bipolar I disorder and n=127 for case control) were collected from individuals unrelated in the southwest of Iran. The SNPs (rs947267 and rs3918342 for DAOA gene/ rs165599 and rs4680 for COMT gene) were genotyped using the PCR-RFLP method. Our finding was studied by logistic regression and Mantel-Haenszel Chi-square tests.
Results: We observed an association in rs3918342, rs165599 and rs4680 single nucleotide polymorphisms and schizophrenia and bipolar I disorder. In addition, our data demonstrated that the rs947267 was related to bipolar I disorder but there was no association between this SNP and schizophrenia.
Conclusion: In conclusion, this result supports the hypothesis that variations in DAOA and COMT genes may play a role in schizophrenia and bipolar disorder.
Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2017/02/1 | Accepted: 2018/05/26 | Published: 2018/11/1

References
1. Aleman, A., Kahn, R. S., & Selten, J. P. (2003). Sex differences in the risk of schizophrenia: Evidence from meta-analysis. Archives of General Psychiatry, 60(6), 565-71. [DOI:10.1001/archpsyc.60.6.565] [PMID] [DOI:10.1001/archpsyc.60.6.565]
2. Alizadeh, F., Tabatabaiefar, M. A., Ghadiri, M., Yekaninejad, M. S., Jalilian, N., & Noori-Daloii, M. R. (2012). Association of P1635 and P1655 Polymorphisms in Dysbindin (DTNBP1) gene with schizophrenia. Acta Neuropsychiatrica, 24(3), 155-9. [DOI:10.1111/j.1601-5215.2011.00598.x] [PMID] [DOI:10.1111/j.1601-5215.2011.00598.x]
3. Amirabadi, M. R. E., Esfahani, S. R., Davari-Ashtiani, R., Khademi, M., Emamalizadeh, B., Movafagh, A., et al. (2015). Monoamine oxidase a gene polymorphisms and bipolar disorder in Iranian population. Iranian Red Crescent Medical Journal, 17(2), 23095. [DOI:10.5812/ircmj.23095] [PMID] [PMCID] [DOI:10.5812/ircmj.23095]
4. Arajärvi, R., Ukkola, J., Haukka, J., Suvisaari, J., Hintikka, J., Partonen, T., et al. (2006). Psychosis among" healthy" siblings of schizophrenia patients. BMC Psychiatry, 6, 6. [DOI:10.1186/1471-244X-6-6] [PMID] [PMCID] [DOI:10.1186/1471-244X-6-6]
5. Austin, J. (2005). Schizophrenia: An update and review. Journal of Genetic Counseling, 14(5), 329-40. [DOI:10.1007/s10897-005-1622-4] [PMID] [DOI:10.1007/s10897-005-1622-4]
6. Badner, J. A., & Gershon, E. S. (2002). Meta-analysis of whole-genome linkage scans of bipolar disorder and schizophrenia. Molecular Psychiatry, 7(4), 405-11. [DOI:10.1038/sj.mp.4001012] [PMID] [DOI:10.1038/sj.mp.4001012]
7. Bass, N. J., Datta, S. R., McQuillin, A., Puri, V., Choudhury, K., Thirumalai, S., et al. (2009). Evidence for the association of the DAOA (G72) gene with schizophrenia and bipolar disorder but not for the association of the DAO gene with schizophrenia. Behavioral and Brain Functions, 5(1), 28. [DOI:10.1186/1744-9081-5-28] [PMID] [PMCID] [DOI:10.1186/1744-9081-5-28]
8. Boks, M. P., Rietkerk, T., van de Beek, M.H., Sommer, I. E., de Koning, T. J., & Kahn, R. S. (2007). Reviewing the role of the genes G72 and DAAO in glutamate neurotransmission in schizophrenia. European Neuropsychopharmacology, 17(9), 567-72. [DOI:10.1016/j.euroneuro.2006.12.003] [PMID] [DOI:10.1016/j.euroneuro.2006.12.003]
9. Chu, C. S., Chow, P. C. K., Cohen Woods, S., Gaysina, D., Tang, K. Y., & McGuffin, P. (2017). The DAOA gene is associated with schizophrenia in the Taiwanese population. Psychiatry Research, 252, 201-7. [DOI:10.1016/j.psychres.2017.03.013] [PMID] [DOI:10.1016/j.psychres.2017.03.013]
10. Chumakov, I., Blumenfeld, M., Guerassimenko, O., Cavarec, L., Palicio, M., Abderrahim, H., et al. (2002). Genetic and physiological data implicating the new human gene G72 and the gene for D-amino acid oxidase in schizophrenia. Proceedings of the National Academy of Sciences, 99(21), 13675-80. [DOI:10.1073/pnas.182412499] [PMID] [PMCID] [DOI:10.1073/pnas.182412499]
11. Cooper, N. D. (2010). Functional intronic polymorphisms: Buried treasure awaiting discovery within our genes. Human Genomics, 4(5), 284-8. [DOI:10.1186/1479-7364-4-5-284] [PMID] [PMCID] [DOI:10.1186/1479-7364-4-5-284]
12. Dashti, S., Aboutaleb, N., & Shahbazi, A. (2013). The effect of leptin on prepulse inhibition in a developmental modelof schizophrenia. Neuroscience Letters, 555, 57-61. [DOI:10.1016/j.neulet.2013.09.027] [PMID] [DOI:10.1016/j.neulet.2013.09.027]
13. Dehghani, R., & Shahbazi, A. (2016). A hypothetical animal model for psychosis based on the silencing of GABAergic system. Journal of Advanced Medical Sciences and Applied Technologies, 2(4), 321-2.
14. Foroughmand, A. M., Haidari, M., Galehdari, H., Pooryasin, A., Kazeminejad, S. R., Hosseini, S., et al. (2010). Association study between schizophrenia and the DISC1 gene polymorphism. The Medical Journal of the Islamic Republic of Iran, 24(1), 29-34.
15. Galehdari, H. (2009). Association between the G1001C polymorphism in the GRIN1 gene promoter and schizophrenia in the Iranian population. Molecular Neuroscience, 38(2), 178-81. [DOI:10.1007/s12031-008-9148-5] [PMID] [DOI:10.1007/s12031-008-9148-5]
16. Galehdari, H., Ajam, T., & Pooryasin, A. (2010). Combined effect of polymorphic sites in the DTNBP1 and GRIN1 genes on schizophrenia. Medical Journal of the Islamic Republic of Iran, 24(1), 5-10.
17. Glatt, S., Faraone, S. & Tsuang, MT. (2003). Association between a functional catechol O-methyltransferase gene polymorphism and schizophrenia: Meta-analysis of case-control and family-based studies. The American Journal of Psychiatry, 160(3), 469-476. [DOI:10.1176/appi.ajp.160.3.469] [PMID] [DOI:10.1176/appi.ajp.160.3.469]
18. Gatt, J. M., Burton, K. L., Williams, L. M., & Schofield, P. R. (2015). Specific and common genes implicated across major mental disorders: A review of meta-analysis studies. Journal of Psychiatric Research, 60, 1-13. [DOI:10.1016/j.jpsychires.2014.09.014] [PMID]
19. Goff, D. C., & Coyle, J. T. (2001). The emerging role of glutamate in the pathophysiology and treatment of schizophrenia. American Journal of Psychiatry, 158(9), 1367-77. [DOI:10.1176/appi.ajp.158.9.1367] [PMID] [DOI:10.1176/appi.ajp.158.9.1367]
20. Harrison, P. J. & Weinberger, D. R. (2005). Schizophrenia genes, gene expression, and neuropathology: On the matter of their convergence. Molecular Psychiatry, 10(1), 40-68. [DOI:10.1038/sj.mp.4001686] [PMID] [DOI:10.1038/sj.mp.4001686]
21. Holtzman, J. N., Lolich, M., Ketter, T. A., Vázquez G. H. (2015). Clinical characteristics of bipolar disorder: A comparative study between Argentina and the United States. International Journal of Bipolar Disorders, 3, 8. [DOI:10.1186/s40345-015-0027-z] [PMID] [PMCID] [DOI:10.1186/s40345-015-0027-z]
22. Howes, O., McCutcheon, R. & Stone J. (2015). Glutamate and dopamine in schizophrenia: An update for the 21st century. Journal of Psychopharmacology, 29(2), 97-115. [DOI:10.1177/0269881114563634] [PMID] [PMCID] [DOI:10.1177/0269881114563634]
23. Hukic, D. S. (2016). Genetic association studies of symptoms, comorbidity and outcome in bipolar disorder and schizophrenia. Solna, Stockholm: Karolinska Institutet. [PMCID] [PMCID]
24. Jagannath, V., Gerstenberg M., Correll CU., Walitza S., & Grünblatt E. (2018). A systematic meta-analysis of the association of Neuregulin 1 (NRG1), D-amino acid Oxidase (DAO), and DAO Activator (DAOA)/G72 polymorphisms with schizophrenia. Journal of Neural Transmission, 125(1), 89-102. [DOI:10.1007/s00702-017-1782-z] [PMID] [DOI:10.1007/s00702-017-1782-z]
25. Jagannath, V., Theodoridou, A., Gerstenberg, M., Franscini, M., Heekeren, K., Correll, C. U., et al. (2017). Prediction analysis for transition to schizophrenia in individuals at clinical high risk for psychosis: The relationship of DAO, DAOA, and NRG1 variants with negative symptoms and cognitive deficits. Frontiers in Psychiatry, 8, 292. [DOI:10.3389/fpsyt.2017.00292] [PMID] [PMCID] [DOI:10.3389/fpsyt.2017.00292]
26. Karayiorgou, M., Morris, M. A., Morrow, B., Shprintzen, R. J., Goldberg, R., Borrow, J., et al. (1995). Schizophrenia susceptibility associated with interstitial deletions of chromosome 22q11. Proceedings of the National Academy of Sciences, 92(17), 7612-6. [PMID] [PMCID] [DOI:10.1073/pnas.92.17.7612]
27. Lajin, B., Alachkar, A., Hamzeh, A. R., Michati, R., & Alhaj, H. (2011). No association between Val158Met of the COMT gene and susceptibility to schizophrenia in the Syrian population. North American Journal of Medicine Science, 3(4), 176-8. [DOI:10.4297/najms.2011.3176] [PMID] [PMCID] [DOI:10.4297/najms.2011.3176]
28. Leahy, R. L. (2007). Bipolar disorder: Causes, contexts, and treatments. Journal of Clinical Psychology, 63(5), 417-24. [DOI:10.1002/jclp.20360] [PMID] [DOI:10.1002/jclp.20360]
29. Lewis, C. M., Levinson, D. F., Wise, L. H., DeLisi, L. E., Straub, R. E., Hovatta, I., et al. (2003). Genome scan meta-analysis of schizophrenia and bipolar disorder, part II: Schizophrenia. The American Journal of Human Genetics, 73(1), 34-48. [DOI:10.1086/376549] [PMID] [PMCID] [DOI:10.1086/376549]
30. Lin, Z., & Li, W. H. (2012). Evolution of 5′ untranslated region length and gene expression reprogramming in yeasts. Molecular Biology and Evolution, 29(1), 81-9. [DOI:10.1093/molbev/msr143] [PMID] [PMCID]
31. Liu, Y. L., Fann, C. S. J., Liu, C. M., Chang, C. C., Wu, J. Y., Hung, S. I., et al. (2006). No association of G72 and D-amino acid oxidase genes with schizophrenia. Schizophrenia Research, 87(1-3), 15-20. [DOI:10.1016/j.schres.2006.06.020] [PMID] [DOI:10.1016/j.schres.2006.06.020]
32. Lobo, A., Pérez Echeverría, M. J., & Artal, J. (1986). Validity of the scaled version of the General Health Questionnaire (GHQ-28) in a Spanish population. Psychological Medicine, 16(1), 135-40. [DOI:10.1017/S0033291700002579] [PMID] [DOI:10.1017/S0033291700002579]
33. Lotta, T., Vidgren, J., Tilgmann, C., Ulmanen, I., Melen, K., Julkunen, I., et al. (1995). Kinetics of human soluble and membrane-bound catechol O-methyltransferase: A revised mechanism and description of the thermolabile variant of the enzyme. Biochemistry, 34(13), 4202-10. [DOI:10.1021/bi00013a008] [PMID] [DOI:10.1021/bi00013a008]
34. Maderia, C., Freitas, M. E., Vargas-Lopes, C., Wolosker, H. & Panizzutti, R. (2008). Increased brain D-Amino Acid Oxidase (DAAO) activity in schizophrenia. Schizophrenia Research, 101(1-3), 76-83. [DOI:10.1016/j.schres.2008.02.002] [PMID] [DOI:10.1016/j.schres.2008.02.002]
35. Meador Woodruff J. & Healy D. (2000). Glutamate receptor expression in schizophrenic brain. Brain Research Reviews, 31(2-3), 288-94. [DOI:10.1016/S0165-0173(99)00044-2] [DOI:10.1016/S0165-0173(99)00044-2]
36. Mynett Johnson, L. A., Murphy, V. E., Claffey, E., Shields, D. C., & McKeon, P. (1998). Preliminary evidence of an association between bipolar disorder in females and the catechol-O-methyltransferase gene. Psychiatric Genetics, 8(4), 221-5. [DOI:10.1097/00041444-199808040-00004] [PMID] [DOI:10.1097/00041444-199808040-00004]
37. Nasirizade, F., Mostofi, M. & Shahbazi, A. (2016). Sensorimotor gating deficit in a developmental model of schizophrenia in male Wistar rats. Journal of Medical Physiology, 2(1), 15-19.
38. Rahman zadeh, S., Mohammadi, H. S, karimipour, M., Heidari keshel, S. & Omidinia, E. (2012). Investigation of genetic association between PRODH gene and schizophrenia in Iranian population. Journal of Paramedic Practice, 3(1), 7-16.
39. Rahmanzadeh, R., Shahbazi, A., Ardakani, M. R. K., Mehrabi, S., Rahmanzade, R., & Joghataei, M. T. (2017). Lack of the effect of bumetanide, a selective NKCC1 inhibitor, in patients with schizophrenia: A double‐blind randomized trial. Psychiatry and Clinical Neurosciences, 71(1), 72-3. [DOI:10.1111/pcn.12475] [PMID] [DOI:10.1111/pcn.12475]
40. Rees, E., O'Donovan, M. C., & Owen, M. J. (2015). Genetics of schizophrenia. Current Opinion in Behavioral Sciences, 2, 8-14. [DOI:10.1016/j.cobeha.2014.07.001] [DOI:10.1016/j.cobeha.2014.07.001]
41. Risch, N. (1990). Linkage strategies for genetically complex traits.I. multilocus models. American-ournal of Human Genetics, 46(2), 222-8. [PMID] [PMCID]
42. Ross, C. A., Margolis, R. L., Reading, S. A., Pletnikov, M., Coyle, J. T. (2006). Neurobiology of schizophrenia. Neuron, 52(1), 139-53. [DOI:10.1016/j.neuron.2006.09.015] [PMID] [DOI:10.1016/j.neuron.2006.09.015]
43. Sacchetti, E., Scassellati, C., Minelli, A., Valsecchi, P., Bonvicini, C., Pasqualetti, P., et al. (2013). Schizophrenia susceptibility and NMDA-receptor mediated signalling: An association study involving 32 tagSNPs of DAO, DAOA, PPP3CC, and DTNBP1 genes. BMC Medical Genetics, 14, 33. [DOI:10.1186/1471-2350-14-33] [PMID] [PMCID] [DOI:10.1186/1471-2350-14-33]
44. Shariati, SAM., Behmanesh, M., & Galehdari, H. (2011). A study of the association between SNP8NRG241930 in the 5' End of Neuroglin 1 gene with schizophrenia in a group of Iranian patients. Cell Journal, 13(2), 91-6.
45. Shi, J., Badner, J. A., Gershon, E. S. & Liu, C. (2008). Allelic association of G72/G30 with schizophrenia and bipolar disorder: A comprehensive meta-analysis. Schizophrenia Research, 98(1-3), 89-97. [DOI:10.1016/j.schres.2007.10.004] [PMID] [PMCID] [DOI:10.1016/j.schres.2007.10.004]
46. Shifman, S., Bronstein, M., Sternfeld, M., Pisanté Shalom, A., Lev Lehman, E., Weizman, A., et al. (2002). A highly significant association between a COMT haplotype and schizophrenia. The American Journal of Human Genetics, 71(6), 1296-1302. [DOI:10.1086/344514] [PMID] [PMCID] [DOI:10.1086/344514]
47. Shifman, S., Bronstein, M., Sternfeld, M., Pisanté, A., Weizman, A., Reznik, I., et al. (2004). COMT: A common susceptibility gene in bipolar disorder and schizophrenia. American Journal of Medical Genetics, 128(1), 61-4. [DOI:10.1002/ajmg.b.30032] [PMID] [DOI:10.1002/ajmg.b.30032]
48. Tan, J., Lin, Y., Su, L., Yan, Y., Chen, Q., Jiang, H., et al. (2014). Association between DAOA gene polymorphisms and the risk of schizophrenia, bipolar disorder and depressive disorder. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 51, 89-98. [DOI:10.1016/j.pnpbp.2014.01.007] [PMID] [DOI:10.1016/j.pnpbp.2014.01.007]
49. Tsai, G., & Coyle, J. T. (2002). Glutamatergic mechanisms in schizophrenia. Annual Review of Pharmacology and Toxicology, 42(1), 165-79. [DOI:10.1146/annurev.pharmtox.42.082701.160735] [PMID] [DOI:10.1146/annurev.pharmtox.42.082701.160735]
50. Yue, W., Kang, G., Zhang, Y., Qu, M., Tang, F., Han, Y., et al. (2007). Association of DAOA polymorphisms with schizophrenia and clinical symptoms or therapeutic effects. Neuroscience Letters, 416(1), 96-100. [DOI:10.1016/j.neulet.2007.01.056] [PMID] [DOI:10.1016/j.neulet.2007.01.056]

Add your comments about this article : Your username or Email:
CAPTCHA

Send email to the article author


© 2019 All Rights Reserved | Basic and Clinical Neuroscience

Designed & Developed by : Yektaweb