腺苷 A2a 受体多态性与焦虑症易感性。

IF 0.8 Q4 CLINICAL NEUROLOGY Iranian Journal of Child Neurology Pub Date : 2024-01-01 Epub Date: 2024-09-29 DOI:10.22037/ijcn.v18i4.43928
Mohammad Keyvanloo Shahrestanaki, Haniyeh Karami, Hadi Lotfi, Milad Khorasani, Zeinab Babaei, Mohammad Salari Zare, Marzieh Kafami, Ilia Abrishami
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引用次数: 0

摘要

焦虑症(ADs)是一组精神障碍,其特征是面对生活经历时感到紧张、恐惧和过度担忧。腺苷 A2a 受体(ADORA2A)的信号传递异常被认为与焦虑症的发病机制有关。ADORA2A 基因的多态性已被证明与注意力缺失症的某些表现形式有关。这些研究的结果并不一致,因此很难得出明确的结论。因此,本研究对 ADORA2A 基因多态性与 ADs 易感性之间的关系进行了系统回顾。本研究使用适当的关键词在 PubMedline/Medline、Web of Science 和 Scopus 数据库中进行检索,然后根据纳入/排除标准筛选出合适的研究。结果发现,ADORA2A的rs5751876(1976T>C或之前的1083C>T)和rs35060421(2592C>Tins)多态性与ADs易感性增加有关。此外,rs2298383 TT基因型可能是致病调控因子,而ADORA2A T/C(rs2298383/rs3761422)单倍型对ADs的发生有显著的易感性。要进一步明确ADORA2A基因多态性在ADs发病机制中的作用,还需要更多的研究。
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Adenosine A2a Receptor Polymorphisms and Susceptibility to Anxiety Disorders.

Anxiety disorders (ADs) are a group of mental disorders characterized by feelings of tension, fear, and excessive worrying in the face of life experiences. Aberrant signaling of adenosine A2a receptor (ADORA2A) is believed to be involved in the pathogenesis of ADs. Polymorphisms in the ADORA2A gene were shown to be associated with some of the patterns presented by ADs. The results of these studies have been inconsistent, making it hard to draw definitive conclusions. Therefore, this study performed a systematic review to clarify the associations between ADORA2A gene polymorphisms and ADs susceptibility. PubMed/Medline, Web of Science, and Scopus database using appropriate keywords, then screened for separation of suitable studies based on inclusion/exclusion criteria. Collectively, rs5751876 (1976T>C or previously 1083C>T) and rs35060421 (2592C>Tins) polymorphisms of ADORA2A were associated with an increased susceptibility to ADs. Moreover, rs2298383 TT genotype may be the causal regulatory factor, and ADORA2A T/C (rs2298383/rs3761422) haplotypes have significant susceptibility to ADs development. Additional research is needed to further define the role of ADORA2A gene polymorphisms in the pathogenesis of ADs.

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