The Association Study of IL-23R Polymorphisms With Cerebral Palsy in Chinese Population

Cerebral palsy (CP) is a syndrome of non-progressive motor dysfunction caused by early brain development injury. Recent evidence has shown that immunological abnormalities are associated with an increased risk of CP. We recruited 782 children with CP as the case group and 770 healthy children as the...

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Veröffentlicht in:FRONTIERS IN NEUROSCIENCE 2020-11, Vol.14, p.590098-590098
Hauptverfasser: Wang, Yangong, Xu, Yiran, Fan, Yangyi, Bi, Dan, Song, Juan, Xia, Lei, Shang, Qing, Gao, Chao, Zhang, Xiaoli, Zhu, Dengna, Qiao, Yimeng, Su, Yu, Wang, Xiaoyang, Zhu, Changlian, Xing, Qinghe
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Sprache:eng
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Zusammenfassung:Cerebral palsy (CP) is a syndrome of non-progressive motor dysfunction caused by early brain development injury. Recent evidence has shown that immunological abnormalities are associated with an increased risk of CP. We recruited 782 children with CP as the case group and 770 healthy children as the control group. The association between single nucleotide polymorphisms (SNPs; namely, rs10889657, rs6682925, rs1884444, rs17375018, rs1004819, rs11805303, and rs10889677) and CP was studied by using a case-control method and SHEsis online software. Subgroup analysis based on complications and clinical subtypes was also carried out. There were differences in the allele and genotype frequencies between CP cases and controls at the rs11805303 and rs10889677 SNPs ( allele = 0.014 and 0.048, respectively; genotype = 0.023 and 0.008, respectively), and the difference in genotype frequency of rs10889677 remained significant after Bonferroni correction ( genotype = 0.048). Subgroup analysis revealed a more significant association of rs10889677 with CP accompanied by global developmental delay ( genotype = 0.024 after correction) and neonatal encephalopathy ( genotype = 0.024 after correction). The present results showed a significant association between and CP, suggesting that may play a potential role in CP pathogenesis.
ISSN:1662-4548
1662-453X
1662-453X
DOI:10.3389/fnins.2020.590098