No associations between five polymorphisms in COMT gene and migraine.

No associations between five polymorphisms in COMT gene and migraine.
复制标题

COMT 基因的五个多态性与偏头痛之间没有关联。

DOI:
10.1111/ane.12583
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发表时间:
2016
期刊:
影响因子:
3.5
通讯作者:
Nakashima K
Nakashima K
中科院分区:
医学3区
文献类型:
--
作者:
Takigawa H;Kowa H;Nakashima K

文献摘要

相似文献

目的偏头痛的病理生理机制尚不清楚。多巴胺能系统已被假设参与偏头痛的发病机制。本研究的目的是调查儿茶酚-O-甲基转移酶(COMT)多态性和慢性头痛。我们分析了5个单核苷酸多态性(SNPs)inCOMT.Materials & MethodsThe研究人群包括71例有先兆偏头痛患者,152例无先兆偏头痛患者,86例紧张型头痛患者和191例健康对照。选择的多态性标记包括一个引起His 62 His(rs 4633)和两个非同义SNP,Ala 72 Ser和Val 158 Met(分别为rs6267,rs 4680)。其他两个非多态性SNPs(rs6270,rs740602)examined.ResultsWe发现在任何基因型,等位基因频率,或单倍型之间的患者groupsand controls.ConclusionsOur的研究结果表明,五个多态性在COMT没有关联偏头痛在日本西部。基因的其他部分可能含有一个负责改变COMT表达或酶活性的突变,这一可能性很重要。我们不能最终排除整个COMT基因参与偏头痛发病机制。
ObjectivesThe pathophysiology of migraine headaches is not clearly understood yet. The dopaminergic system has been hypothesized to be involved in migraine pathogenesis. The aim of this study was to investigate catechol‐O‐methyltransferase (COMT) polymorphisms and chronic headaches. We analyzed five single nucleotide polymorphisms (SNPs) inCOMT.Materials & MethodsThe study population consisted of 71 patients with migraine with aura, 152 patients with migraine without aura, 86 patients with tension‐type headache, and 191 healthy controls. The selected polymorphic markers included one causing His62His (rs4633) and two non‐synonymous SNPs, Ala72Ser and Val158Met (rs6267, rs4680 respectively). Two other non‐polymorphic SNPs (rs6270, rs740602) were examined.ResultsWe found no significant differences in any genotypes, allele frequencies, or haplotypes among the patient groups and controls.ConclusionsOur results indicate that the five polymorphisms inCOMThave no association with migraineurs in Western Japan. The possibility that segments elsewhere in the gene may contain a mutation responsible for modifying the expression ofCOMTor the activity of the enzyme is important. We cannot conclusively exclude the entire COMT gene from being involved in migraine pathogenesis.