BibTex RIS Kaynak Göster

Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi

Yıl 2016, Cilt: 43 Sayı: 2, 218 - 223, 01.06.2016

Öz

Amaç: Bu çalışmanın amacı, adenozin deaminaz (ADA)
genindeki G22A polimorfizminin Türk popülasyonunda şizofreni
ile ilişkisinin araştırılmasıdır.
Yöntemler: Bu çalışmada biz 113 şizofreni tanısı almış
hasta ve 121 sağlıklı kontrol bireylerini inceledik. ADA
geni G22A polimorfizmi allel spesifik-polimeraz zincir reaksiyonu
(AS-PCR) yöntemi kullanılarak belirlendi.
Bulgular: ADA genindeki G22A polimorfizmi için GG,
GA ve AA genotip sıklıkları sırası ile kontrol grubu için
%79.3 (96/121), %20,3 (25/121), %0 (0) ve hasta grubu
için %87,6 (99/113), %10,6 (12/113), %1,8 (2/113) olarak
belirlendi. Genotip dağılım bakımından hasta ve kontrol
grupları arasında anlamlı fark bulundu (p=0,017). Ayrıca
GA genotipinin sıklığı hastalarda kontrole nazaran anlamlı
düzeyde düşük bulundu (p=0,048, OR=0.46, 95%CI 0.22-
0.96). Fakat allel sıklıkları bakımından iki grup arasında
anlamlı fark bulunamadı. Cinsiyet bakımından karşılaştırma
yaptığımız zaman, erkek hastalarda GG genotipinin
anlamlı düzeyde yüksek, GA genotipinin ise düşük olduğu
gözlendi (sırası ile p=0,036 ve p=0,005). Kadın hastalarda
herhangi bir anlamlı fark gözlenmedi.
Sonuç: Bizim sonuçlar ADA genindeki G22A polimorfizminin
Türk popülasyonunda şizofreni hastalığı ile ilişkili
olabileceğini gösterdi. ADA genindeki GA genotipinin
özellikle erkeklerde şizofreniye yatkınlığı düşürdüğü,
buna karşın GG genotipinin yatkınlığı arttırdığı muhtemeldir.
Farklı hasta ve etnik gruplar ile gelecekte yapılacak
çalışmalar, elde ettiğimiz sonuçların kesinleşmesine
yardımcı olur

Kaynakça

  • 1. Zhang L, Zhong X, An Z, et al. Association analysis of the GRM8 gene with schizophrenia in the Uygur Chinese population. Hereditas 2014;151:140-144.
  • 2. El-Hadidy MA, Abdeen HM, Abd El-Aziz SM, et al. MTHFR gene polymorphism and age of onset of schizophrenia and bipolar disorder. Biomed Res Int 2014;2014:318483.
  • 3. Dutra GP, Ottoni GL, Lara DR, et al. Lower frequency of the low activity adenosine deaminase allelic variant (ADA1*2) in schizophrenic patients. Rev Bras Psiquiatr 2010;32:275- 278.
  • 4. Nunes DP, Spegiorin LC, Mattos CC, et al. The ADA*2 allele of the adenosine deaminase gene (20q13.11) and recurrent spontaneous abortions: an age-dependent association. Clinics (Sao Paulo) 2011;66:1929-1933.
  • 5. Hettinger JA, Liu X, Holden JJ. The G22A polymorphism of the ADA gene and susceptibility to autism spectrum disorders. J Autism Dev Disord 2008;38:14-19.
  • 6. Takhshid MA, Zahediannejad Z, Aboualizadeh F, et al. G22A Polymorphism of adenosine deaminase and its association with biochemical characteristics of gestational diabetes mellitus in an Iranian population. Iran J Med Sci. 2015;40:170-174.
  • 7. Camargo U, Toledo RA, Cintra JR, et al. Lack of association of the G22A polymorphism of the ADA gene in patients with ankylosing spondylitis. Genet Mol Res 2012;11:1178- 1184.
  • 8. Battistuzzi G, Iudicone P, Santolamazza P, et al. Activity of adenosine deaminase allelic forms in intact erythrocytes and in lymphocytes. Ann Hum Genet 1981;45:15-19.
  • 9. Washington, DC: American Psychiatric Association; 2000. American Psychiatric Association, editor. Diagnostic and Statistical Manual of Mental Disorders.
  • 10. Sun YJ, Yu Y, Zhu GC, et al. Association between single nucleotide polymorphisms in MiR219-1 and MiR137 and susceptibility to schizophrenia in a Chinese population. FEBS Open Bio 2015;5:774-778.
  • 11. Consortium. Schizophrenia Working Group of the Psychiatric Genomics Biological insights from 108 schizophreniaassociated genetic loci. Nature 2014;511:421-427.
  • 12. Schmidt A, Böhmer AE, Antunes C, et al. Anti-nociceptive properties of the xanthine oxidase inhibitor allopurinol in mice: role of A1 adenosine receptors. Br J Pharmacol 2009;156:163-172.
  • 13. Brunstein MG, Ghisolfi ES, Ramos FL, et al. A clinical trial of adjuvant allopurinol therapy for moderately refractory schizophrenia. J Clin Psychiatry 2005;66:213-219.
  • 14 .Boison D, Singer P, Shen HY, et al. Adenosine hypothesis of schizophrenia--opportunities for pharmacotherapy. Neuropharmacology. 2012;62:1527-1543.
  • 15. Demirci K, Özçankaya R, Yilmaz HR, et al. Paliperidone regulates intracellular redox system in rat brain: Role of purine mechanism. Redox Rep 2015;20:170-6.
  • 16. Lara DR, Dall’Igna OP, Ghisolfi ES, et al. Involvement of adenosine in the neurobiology of schizophrenia and its therapeutic implications. Prog Neuropsychopharmacol Biol Psychiatry 2006;30:617-629.
  • 17. Sebastião AM, Ribeiro JA. Adenosine receptors and the central nervous system. Handb Exp Pharmacol 2009;193:471– 534.
  • 18. Shen HY, Singer P, Lytle N, et al. Adenosine augmentation ameliorates psychotic and cognitive endophenotypes of schizophrenia. J Clin Invest 2012;122:2567-2577.
  • 19. Akkoç H, Kelle I, Kale E, et al. The Effects of Ischemic Preconditioning on Cardiac Ischemia-Reperfusion Injury in Rat Lung. Dicle Med J 2008;35:102-109.
  • 20. Boison D. Modulators of nucleoside metabolism in the therapy of brain diseases.Curr Top Med Chem. 2011;11:1068- 1086.
  • 21. Yee BK, Singer P, Chen JF, et al. Transgenic overexpression of adenosine kinase in brain leads to multiple learning impairments and altered sensitivity to psychomimetic drugs. Eur J Neurosci. 2007;26:3237-3252.
  • 22. Gotoh L, Mitsuyasu H, Kobayashi Y, et al. Association analysis of adenosine A1 receptor gene (ADORA1) polymorphisms with schizophrenia in a Japanese population. Psychiatr Genet. 2009;19:328-335.
  • 23. Lalande D, Thériault L, Kalinova É, et al. The effect of exercise on sleep quality and psychological, physiological, and biological correlates in patients with schizophrenia: A pilot study. Schizophr Res 2016;Mar;171:235-236.
  • 24. Garcia-Rill E, D’Onofrio S, Mahaffey S, et al. Pedunculopontine arousal system physiology-Implications for schizophrenia. Sleep Sci 2015;8:82-91.
  • 25. Basheer R, Strecker RE, Thakkar MM, et al. Adenosine and sleepwake regulation. Prog Neurobiol 2004;73:379-396.
  • 26. Rétey JV, Adam M, Honegger E, et al. A functional genetic variation of adenosine deaminase affects the duration and intensity of deep sleep in humans. Proc Natl Acad Sci USA 2005;102:15676-15681.
  • 27. Stubbs G, Litt M, Lis E, J et al. Adenosine deaminase activity decreased in autism. J Am Acad Child Psychiatry 1982;21:71-74.
  • 28. Zoroglu SS, Armutcu F, Ozen S, et al. Increased oxidative stress and altered activities of erythrocyte free radical scavenging enzymes in autism. Eur Arch Psychiatry Clin Neurosci 2004;254:143-147.
  • 29. Herken H, Akyol O, Yilmaz HR, et al. Nitric oxide, adenosine deaminase, xanthine oxidase and superoxide dismutase in patients with panic disorder: alterations by antidepressant treatment. Hum Psychopharmacol 2006;21:53-59.
  • 30. Yolaç Yarpuz A, Yilmaz A, et al. Levels of adenosine deaminase and dipeptidyl peptidase IV in patients with panic disorder .Turk Psikiyatri Derg. 2008;19:149-156.
  • 31. Herken H, Gurel A, Selek S, et al. Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment. Arch Med Res. 2007;38:247-252.
  • 32. Elgün S, Keskinege A, Kumbasar H. Dipeptidyl peptidase IV and adenosine deaminase activity. Decrease in depression. Psychoneuroendocrinology 1999;24:823-832.
  • 33. Brunstein MG, Silveira EM Jr, Chaves LS, et al. Increased serum adenosine deaminase activity in schizophrenic receiving antipsychotic treatment. Neurosci Lett 2007;414:61-64.
  • 34. Concetti F, Carpi FM, Nabissi M, et al. The functional polymorphism rs73598374:G>A (p.Asp8Asn) of the ADA gene is associated with telomerase activity and leukocyte telomere length. Eur J Hum Genet 2015;23:267-270.
  • 35. Bottini N, De Luca D, Saccucci P, et al. Autism: evidence of association with adenosine deaminase genetic polymorphism. Neurogenetics 2001;3:111-113.
  • 36. Tavilani H, Sheikh N, Vaisi-raygani A, et al. Sex differences in adenosine deaminase activity of stroke patients. Clin Chem Lab Med. 2008;46:506-509.
  • 37. Brann DW, Dhandapani K, Wakade C, et al. Neurotrophic and neuroprotective actions of estrogen: basic mechanisms and clinical implications. Steroids 2007;72:381–405.

Adenosine Deaminase Gene G22a Polymorphism as a Risk Factor for Schizophrenia in Turkish Population

Yıl 2016, Cilt: 43 Sayı: 2, 218 - 223, 01.06.2016

Öz

Objective: The aim of this study was to investigate whether the G22A polymorphism of adenosine deami­nase (ADA) gene is associated with schizophrenia in Turkish population. Methods: In this study, we evaluated 113 patients with schizophrenia and 121 individuals without the disease. The ADA G22A polymorphism was examined using allele specific-polymerase chain reaction (PCR). Results: The ADA G22A genotype frequencies of GG, GA, and AA were 79.3% (96/121), 20.7% (25/121) and 0% (0) in the control group, while 87.6 % (99/113), 10.6% (12/113), 1.8% (2/113) in the patient group, respectively. There was a statistically significant difference in genotype distribution between patients and controls (p=0.017). Also the frequency of GA genotype was found significantly low­er in patients compared with healthy controls (OR = 0.46, 95% Cl 0.22-0.96, p =0.048). However, there was not any noticeable difference in allele distribution between the groups (p>0.05). In addition, the frequency of GG geno­type in the male patient group significantly higher, and GA genotype significantly lower compared to the male control group, were found (p=0.036, p=0.005, respectively). No association was found for the female group. Conclusion: Our results show that, the G22A polymor­phism of ADA gene may be associated with schizophrenia in Turkish population. The ADA GA genotype is likely to reduce, whereas GG genotype increased genetic sus­ceptibility to schizophrenia, especially in males. Further studies should be repeated with different study subjects and/or other ethnic subjects to generalize the conclusion of this study.

Kaynakça

  • 1. Zhang L, Zhong X, An Z, et al. Association analysis of the GRM8 gene with schizophrenia in the Uygur Chinese population. Hereditas 2014;151:140-144.
  • 2. El-Hadidy MA, Abdeen HM, Abd El-Aziz SM, et al. MTHFR gene polymorphism and age of onset of schizophrenia and bipolar disorder. Biomed Res Int 2014;2014:318483.
  • 3. Dutra GP, Ottoni GL, Lara DR, et al. Lower frequency of the low activity adenosine deaminase allelic variant (ADA1*2) in schizophrenic patients. Rev Bras Psiquiatr 2010;32:275- 278.
  • 4. Nunes DP, Spegiorin LC, Mattos CC, et al. The ADA*2 allele of the adenosine deaminase gene (20q13.11) and recurrent spontaneous abortions: an age-dependent association. Clinics (Sao Paulo) 2011;66:1929-1933.
  • 5. Hettinger JA, Liu X, Holden JJ. The G22A polymorphism of the ADA gene and susceptibility to autism spectrum disorders. J Autism Dev Disord 2008;38:14-19.
  • 6. Takhshid MA, Zahediannejad Z, Aboualizadeh F, et al. G22A Polymorphism of adenosine deaminase and its association with biochemical characteristics of gestational diabetes mellitus in an Iranian population. Iran J Med Sci. 2015;40:170-174.
  • 7. Camargo U, Toledo RA, Cintra JR, et al. Lack of association of the G22A polymorphism of the ADA gene in patients with ankylosing spondylitis. Genet Mol Res 2012;11:1178- 1184.
  • 8. Battistuzzi G, Iudicone P, Santolamazza P, et al. Activity of adenosine deaminase allelic forms in intact erythrocytes and in lymphocytes. Ann Hum Genet 1981;45:15-19.
  • 9. Washington, DC: American Psychiatric Association; 2000. American Psychiatric Association, editor. Diagnostic and Statistical Manual of Mental Disorders.
  • 10. Sun YJ, Yu Y, Zhu GC, et al. Association between single nucleotide polymorphisms in MiR219-1 and MiR137 and susceptibility to schizophrenia in a Chinese population. FEBS Open Bio 2015;5:774-778.
  • 11. Consortium. Schizophrenia Working Group of the Psychiatric Genomics Biological insights from 108 schizophreniaassociated genetic loci. Nature 2014;511:421-427.
  • 12. Schmidt A, Böhmer AE, Antunes C, et al. Anti-nociceptive properties of the xanthine oxidase inhibitor allopurinol in mice: role of A1 adenosine receptors. Br J Pharmacol 2009;156:163-172.
  • 13. Brunstein MG, Ghisolfi ES, Ramos FL, et al. A clinical trial of adjuvant allopurinol therapy for moderately refractory schizophrenia. J Clin Psychiatry 2005;66:213-219.
  • 14 .Boison D, Singer P, Shen HY, et al. Adenosine hypothesis of schizophrenia--opportunities for pharmacotherapy. Neuropharmacology. 2012;62:1527-1543.
  • 15. Demirci K, Özçankaya R, Yilmaz HR, et al. Paliperidone regulates intracellular redox system in rat brain: Role of purine mechanism. Redox Rep 2015;20:170-6.
  • 16. Lara DR, Dall’Igna OP, Ghisolfi ES, et al. Involvement of adenosine in the neurobiology of schizophrenia and its therapeutic implications. Prog Neuropsychopharmacol Biol Psychiatry 2006;30:617-629.
  • 17. Sebastião AM, Ribeiro JA. Adenosine receptors and the central nervous system. Handb Exp Pharmacol 2009;193:471– 534.
  • 18. Shen HY, Singer P, Lytle N, et al. Adenosine augmentation ameliorates psychotic and cognitive endophenotypes of schizophrenia. J Clin Invest 2012;122:2567-2577.
  • 19. Akkoç H, Kelle I, Kale E, et al. The Effects of Ischemic Preconditioning on Cardiac Ischemia-Reperfusion Injury in Rat Lung. Dicle Med J 2008;35:102-109.
  • 20. Boison D. Modulators of nucleoside metabolism in the therapy of brain diseases.Curr Top Med Chem. 2011;11:1068- 1086.
  • 21. Yee BK, Singer P, Chen JF, et al. Transgenic overexpression of adenosine kinase in brain leads to multiple learning impairments and altered sensitivity to psychomimetic drugs. Eur J Neurosci. 2007;26:3237-3252.
  • 22. Gotoh L, Mitsuyasu H, Kobayashi Y, et al. Association analysis of adenosine A1 receptor gene (ADORA1) polymorphisms with schizophrenia in a Japanese population. Psychiatr Genet. 2009;19:328-335.
  • 23. Lalande D, Thériault L, Kalinova É, et al. The effect of exercise on sleep quality and psychological, physiological, and biological correlates in patients with schizophrenia: A pilot study. Schizophr Res 2016;Mar;171:235-236.
  • 24. Garcia-Rill E, D’Onofrio S, Mahaffey S, et al. Pedunculopontine arousal system physiology-Implications for schizophrenia. Sleep Sci 2015;8:82-91.
  • 25. Basheer R, Strecker RE, Thakkar MM, et al. Adenosine and sleepwake regulation. Prog Neurobiol 2004;73:379-396.
  • 26. Rétey JV, Adam M, Honegger E, et al. A functional genetic variation of adenosine deaminase affects the duration and intensity of deep sleep in humans. Proc Natl Acad Sci USA 2005;102:15676-15681.
  • 27. Stubbs G, Litt M, Lis E, J et al. Adenosine deaminase activity decreased in autism. J Am Acad Child Psychiatry 1982;21:71-74.
  • 28. Zoroglu SS, Armutcu F, Ozen S, et al. Increased oxidative stress and altered activities of erythrocyte free radical scavenging enzymes in autism. Eur Arch Psychiatry Clin Neurosci 2004;254:143-147.
  • 29. Herken H, Akyol O, Yilmaz HR, et al. Nitric oxide, adenosine deaminase, xanthine oxidase and superoxide dismutase in patients with panic disorder: alterations by antidepressant treatment. Hum Psychopharmacol 2006;21:53-59.
  • 30. Yolaç Yarpuz A, Yilmaz A, et al. Levels of adenosine deaminase and dipeptidyl peptidase IV in patients with panic disorder .Turk Psikiyatri Derg. 2008;19:149-156.
  • 31. Herken H, Gurel A, Selek S, et al. Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment. Arch Med Res. 2007;38:247-252.
  • 32. Elgün S, Keskinege A, Kumbasar H. Dipeptidyl peptidase IV and adenosine deaminase activity. Decrease in depression. Psychoneuroendocrinology 1999;24:823-832.
  • 33. Brunstein MG, Silveira EM Jr, Chaves LS, et al. Increased serum adenosine deaminase activity in schizophrenic receiving antipsychotic treatment. Neurosci Lett 2007;414:61-64.
  • 34. Concetti F, Carpi FM, Nabissi M, et al. The functional polymorphism rs73598374:G>A (p.Asp8Asn) of the ADA gene is associated with telomerase activity and leukocyte telomere length. Eur J Hum Genet 2015;23:267-270.
  • 35. Bottini N, De Luca D, Saccucci P, et al. Autism: evidence of association with adenosine deaminase genetic polymorphism. Neurogenetics 2001;3:111-113.
  • 36. Tavilani H, Sheikh N, Vaisi-raygani A, et al. Sex differences in adenosine deaminase activity of stroke patients. Clin Chem Lab Med. 2008;46:506-509.
  • 37. Brann DW, Dhandapani K, Wakade C, et al. Neurotrophic and neuroprotective actions of estrogen: basic mechanisms and clinical implications. Steroids 2007;72:381–405.
Toplam 37 adet kaynakça vardır.

Ayrıntılar

Diğer ID JA28CF49CU
Bölüm Araştırma Makalesi
Yazarlar

Aydın Rüstemoğlu Bu kişi benim

Birgül Elbozan Cumurcu Bu kişi benim

Ayşe Feyda Nursal Bu kişi benim

Mahmut Balkan Bu kişi benim

Melike Uzun Bu kişi benim

Serbülent Yiğit Bu kişi benim

Yayımlanma Tarihi 1 Haziran 2016
Gönderilme Tarihi 1 Haziran 2016
Yayımlandığı Sayı Yıl 2016 Cilt: 43 Sayı: 2

Kaynak Göster

APA Rüstemoğlu, A., Elbozan Cumurcu, B., Nursal, A. F., Balkan, M., vd. (2016). Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi. Dicle Tıp Dergisi, 43(2), 218-223.
AMA Rüstemoğlu A, Elbozan Cumurcu B, Nursal AF, Balkan M, Uzun M, Yiğit S. Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi. diclemedj. Haziran 2016;43(2):218-223.
Chicago Rüstemoğlu, Aydın, Birgül Elbozan Cumurcu, Ayşe Feyda Nursal, Mahmut Balkan, Melike Uzun, ve Serbülent Yiğit. “Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi”. Dicle Tıp Dergisi 43, sy. 2 (Haziran 2016): 218-23.
EndNote Rüstemoğlu A, Elbozan Cumurcu B, Nursal AF, Balkan M, Uzun M, Yiğit S (01 Haziran 2016) Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi. Dicle Tıp Dergisi 43 2 218–223.
IEEE A. Rüstemoğlu, B. Elbozan Cumurcu, A. F. Nursal, M. Balkan, M. Uzun, ve S. Yiğit, “Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi”, diclemedj, c. 43, sy. 2, ss. 218–223, 2016.
ISNAD Rüstemoğlu, Aydın vd. “Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi”. Dicle Tıp Dergisi 43/2 (Haziran 2016), 218-223.
JAMA Rüstemoğlu A, Elbozan Cumurcu B, Nursal AF, Balkan M, Uzun M, Yiğit S. Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi. diclemedj. 2016;43:218–223.
MLA Rüstemoğlu, Aydın vd. “Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi”. Dicle Tıp Dergisi, c. 43, sy. 2, 2016, ss. 218-23.
Vancouver Rüstemoğlu A, Elbozan Cumurcu B, Nursal AF, Balkan M, Uzun M, Yiğit S. Türk Populasyonunda Şizofreni Hastalığı İçin Bir Risk Faktörü Olarak Adenozin Deaminaz Geni G22a Polimorfizmi. diclemedj. 2016;43(2):218-23.