IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease.
Associations between interleukin 6 (IL-6) polymorphisms and Alzheimer's disease (AD) remain controversial and ambiguous. The aim of this meta-analysis is to explore more precise estimations for the relationship between IL-6-174 G/C and -572 C/G polymorphisms and risk for AD. Electronic searches...
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oai:doaj.org-article:324618e5202340438d0ff8f57d055c3e2021-11-18T07:16:14ZIL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease.1932-620310.1371/journal.pone.0037858https://doaj.org/article/324618e5202340438d0ff8f57d055c3e2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22701584/?tool=EBIhttps://doaj.org/toc/1932-6203Associations between interleukin 6 (IL-6) polymorphisms and Alzheimer's disease (AD) remain controversial and ambiguous. The aim of this meta-analysis is to explore more precise estimations for the relationship between IL-6-174 G/C and -572 C/G polymorphisms and risk for AD. Electronic searches for all publications in databases PubMed and EMBASE were conducted on the associations between IL-6 polymorphisms and risk for AD until January 2012. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated using fixed and random effects models. Twenty-seven studies were included with a total of 19,135 individuals, involving 6,632 AD patients and 12,503 controls. For IL-6-174 G/C polymorphism, the combined results showed significant differences in recessive model (CC vs. CG+GG: OR = 0.65, 95%CI = 0.52-0.82). As regards IL-6-572 C/G polymorphism, significant associations were shown in dominant model (CG+GG vs. CC: OR= 0.73, 95% CI = 0.62-0.86) and in additive model (GG vs. CC, OR= 0.66, 95% CI = 0.46-0.96). In conclusion, genotype CC of IL-6-174 G/C and genotype GG plus GC of IL-6-572 C/G could decrease the risk of AD.Hui-Ping QiZheng-Yi QuShu-Rong DuanShu-Qin WeiShi-Rong WenSheng BiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 6, p e37858 (2012) |
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Medicine R Science Q Hui-Ping Qi Zheng-Yi Qu Shu-Rong Duan Shu-Qin Wei Shi-Rong Wen Sheng Bi IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease. |
description |
Associations between interleukin 6 (IL-6) polymorphisms and Alzheimer's disease (AD) remain controversial and ambiguous. The aim of this meta-analysis is to explore more precise estimations for the relationship between IL-6-174 G/C and -572 C/G polymorphisms and risk for AD. Electronic searches for all publications in databases PubMed and EMBASE were conducted on the associations between IL-6 polymorphisms and risk for AD until January 2012. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated using fixed and random effects models. Twenty-seven studies were included with a total of 19,135 individuals, involving 6,632 AD patients and 12,503 controls. For IL-6-174 G/C polymorphism, the combined results showed significant differences in recessive model (CC vs. CG+GG: OR = 0.65, 95%CI = 0.52-0.82). As regards IL-6-572 C/G polymorphism, significant associations were shown in dominant model (CG+GG vs. CC: OR= 0.73, 95% CI = 0.62-0.86) and in additive model (GG vs. CC, OR= 0.66, 95% CI = 0.46-0.96). In conclusion, genotype CC of IL-6-174 G/C and genotype GG plus GC of IL-6-572 C/G could decrease the risk of AD. |
format |
article |
author |
Hui-Ping Qi Zheng-Yi Qu Shu-Rong Duan Shu-Qin Wei Shi-Rong Wen Sheng Bi |
author_facet |
Hui-Ping Qi Zheng-Yi Qu Shu-Rong Duan Shu-Qin Wei Shi-Rong Wen Sheng Bi |
author_sort |
Hui-Ping Qi |
title |
IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease. |
title_short |
IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease. |
title_full |
IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease. |
title_fullStr |
IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease. |
title_full_unstemmed |
IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer's disease. |
title_sort |
il-6-174 g/c and -572 c/g polymorphisms and risk of alzheimer's disease. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2012 |
url |
https://doaj.org/article/324618e5202340438d0ff8f57d055c3e |
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