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Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia
BACKGROUND: Schizophrenia is one of the most common devastating psychiatric disorders that negatively affects the quality of life and psychosocial functions. Its etiology involves the interplay of complex polygenic influences and environmental risk factors. Inflammatory markers are well-known etiolo...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5396949/ https://www.ncbi.nlm.nih.gov/pubmed/28442912 http://dx.doi.org/10.2147/NDT.S131144 |
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author | Kadasah, Saeed Arfin, Misbahul Rizvi, Sadaf Al-Asmari, Mohammed Al-Asmari, Abdulrahman |
author_facet | Kadasah, Saeed Arfin, Misbahul Rizvi, Sadaf Al-Asmari, Mohammed Al-Asmari, Abdulrahman |
author_sort | Kadasah, Saeed |
collection | PubMed |
description | BACKGROUND: Schizophrenia is one of the most common devastating psychiatric disorders that negatively affects the quality of life and psychosocial functions. Its etiology involves the interplay of complex polygenic influences and environmental risk factors. Inflammatory markers are well-known etiological factors for psychiatric disorders, including schizophrenia. OBJECTIVE: The aim of this study was to investigate the association of proinflammatory cytokine genes, tumor necrosis factor (TNF)-α (−308G/A) and TNF-β (+252A/G) polymorphisms with schizophrenia susceptibility. SUBJECTS AND METHODS: TNF-α and TNF-β genes were amplified using amplification refractory mutation system primers in 180 schizophrenia patients and 200 healthy matched controls recruited from the Psychiatry Clinic of Prince Sultan Military Medical City, Riyadh. The frequencies of alleles and genotypes of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms in patients were compared with those in controls. RESULTS: The frequencies of TNF-α (−308) allele A and genotype GA were significantly higher, while those of allele G and genotype GG were lower in schizophrenia patients as compared to controls, indicating that genotype GA and allele A of TNF-α (−308G/A) may increase susceptibility to schizophrenia, while genotype GG and allele G may reduce it. On the other hand, the distribution of alleles and genotypes of TNF-β (+252A/G) polymorphism does not differ significantly in patients from controls; however, the frequency of genotype GG of TNF-β (+252A/G) was significantly higher in male patients than in female patients. The distribution of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms was almost similar in schizophrenia patients with negative or positive symptoms. CONCLUSION: TNF-α (−308G/A) and TNF-β (+252G/A) polymorphisms may increase the susceptibility to schizophrenia in Saudi patients and could be a potential risk factor for its etiopathogenesis. However, further studies are warranted involving a larger sample size to strengthen our findings. |
format | Online Article Text |
id | pubmed-5396949 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-53969492017-04-25 Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia Kadasah, Saeed Arfin, Misbahul Rizvi, Sadaf Al-Asmari, Mohammed Al-Asmari, Abdulrahman Neuropsychiatr Dis Treat Original Research BACKGROUND: Schizophrenia is one of the most common devastating psychiatric disorders that negatively affects the quality of life and psychosocial functions. Its etiology involves the interplay of complex polygenic influences and environmental risk factors. Inflammatory markers are well-known etiological factors for psychiatric disorders, including schizophrenia. OBJECTIVE: The aim of this study was to investigate the association of proinflammatory cytokine genes, tumor necrosis factor (TNF)-α (−308G/A) and TNF-β (+252A/G) polymorphisms with schizophrenia susceptibility. SUBJECTS AND METHODS: TNF-α and TNF-β genes were amplified using amplification refractory mutation system primers in 180 schizophrenia patients and 200 healthy matched controls recruited from the Psychiatry Clinic of Prince Sultan Military Medical City, Riyadh. The frequencies of alleles and genotypes of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms in patients were compared with those in controls. RESULTS: The frequencies of TNF-α (−308) allele A and genotype GA were significantly higher, while those of allele G and genotype GG were lower in schizophrenia patients as compared to controls, indicating that genotype GA and allele A of TNF-α (−308G/A) may increase susceptibility to schizophrenia, while genotype GG and allele G may reduce it. On the other hand, the distribution of alleles and genotypes of TNF-β (+252A/G) polymorphism does not differ significantly in patients from controls; however, the frequency of genotype GG of TNF-β (+252A/G) was significantly higher in male patients than in female patients. The distribution of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms was almost similar in schizophrenia patients with negative or positive symptoms. CONCLUSION: TNF-α (−308G/A) and TNF-β (+252G/A) polymorphisms may increase the susceptibility to schizophrenia in Saudi patients and could be a potential risk factor for its etiopathogenesis. However, further studies are warranted involving a larger sample size to strengthen our findings. Dove Medical Press 2017-04-12 /pmc/articles/PMC5396949/ /pubmed/28442912 http://dx.doi.org/10.2147/NDT.S131144 Text en © 2017 Kadasah et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Kadasah, Saeed Arfin, Misbahul Rizvi, Sadaf Al-Asmari, Mohammed Al-Asmari, Abdulrahman Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia |
title | Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia |
title_full | Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia |
title_fullStr | Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia |
title_full_unstemmed | Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia |
title_short | Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with schizophrenia |
title_sort | tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in saudi patients with schizophrenia |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5396949/ https://www.ncbi.nlm.nih.gov/pubmed/28442912 http://dx.doi.org/10.2147/NDT.S131144 |
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