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速激肽1(TAC1)基因单核苷酸多态性及单倍型与自闭症的病例对照研究

Tachykinin 1 (TAC1) gene SNPs and haplotypes with autism: a case-control study.

作者信息

Marui Tetsuya, Funatogawa Ikuko, Koishi Shinko, Yamamoto Kenji, Matsumoto Hideo, Hashimoto Ohiko, Nanba Eiji, Nishida Hisami, Sugiyama Toshiro, Kasai Kiyoto, Watanabe Keiichiro, Kano Yukiko, Kato Nobumasa, Sasaki Tsukasa

机构信息

Department of Neuropsychiatry, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.

出版信息

Brain Dev. 2007 Sep;29(8):510-3. doi: 10.1016/j.braindev.2007.01.010. Epub 2007 Mar 21.

Abstract

Autism (MIM 209850) is a severe neurodevelopmental disorder characterized by disturbances in social interaction and communication, by repetitive body movements and restricted interests, and by atypical language development. Several twin and family studies have shown strong evidence for genetic factors in the etiology of autism. Glutamate is a major excitatory neurotransmitter in the human brain. Glutamate systems are involved in the pathophysiology of autism. There are many similarities between the symptoms evoked by glutamate antagonist treatment and symptoms of autism found in several human and animal studies. To elucidate the genetic background of autism, we analyzed the relationship between three single nucleotide polymorphisms (SNPs) of the Tachykinin 1 gene (TAC1) and autism, because TAC1 is located in the candidate region for autism and produces substance P and neurokinins. These products modulate glutamatergic excitatory synaptic transmission and are also involved in inflammation. Many different inflammation-related mechanisms could be involved in the autistic brain. Therefore, TAC1 may have some functions associated with the presumable pathophysiology of autism. We compared the allele and haplotype frequencies between autistic patients (n=170) and normal controls (n=214) in the Japanese population, but no significant difference was observed. Thus, the TAC1 locus is not likely to play a major role in the development of autism.

摘要

自闭症(MIM 209850)是一种严重的神经发育障碍,其特征为社交互动和沟通障碍、重复性身体动作和兴趣受限以及非典型语言发育。多项双胞胎和家族研究有力证明了自闭症病因中的遗传因素。谷氨酸是人类大脑中的主要兴奋性神经递质。谷氨酸系统参与自闭症的病理生理学过程。在多项人类和动物研究中,谷氨酸拮抗剂治疗引发的症状与自闭症症状之间存在许多相似之处。为阐明自闭症的遗传背景,我们分析了速激肽1基因(TAC1)的三个单核苷酸多态性(SNP)与自闭症之间的关系,因为TAC1位于自闭症候选区域,可产生P物质和神经激肽。这些产物调节谷氨酸能兴奋性突触传递,也参与炎症反应。许多不同的炎症相关机制可能与自闭症大脑有关。因此,TAC1可能具有一些与自闭症推测病理生理学相关的功能。我们比较了日本人群中自闭症患者(n = 170)和正常对照(n = 214)之间的等位基因和单倍型频率,但未观察到显著差异。因此,TAC1基因座不太可能在自闭症的发生发展中起主要作用。

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