测试人类焦虑和小鼠焦虑模型先前涉及的基因之间的关联。

IF 2.4 4区 心理学 Q2 BEHAVIORAL SCIENCES
Maizy S. Brasher, Travis J. Mize, Aimee L. Thomas, Charles A. Hoeffer, Marissa A. Ehringer, Luke M. Evans
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引用次数: 0

摘要

焦虑症很常见,可能会使人衰弱,对潜在遗传病因的不完全理解仍然阻碍了有效的治疗。在理解遗传对小鼠焦虑行为模型的影响方面已经取得了进展,但尚不清楚在这些实验系统中鉴定的基因在多大程度上导致了人类焦虑表型的遗传变异。利用新的和现有的大规模人类全基因组关联研究,我们测试了先前在小鼠焦虑样行为研究中发现的一组基因是否会导致一系列人类焦虑症。当作为单个基因进行测试时,13个小鼠鉴定的基因与人类焦虑表型相关,这表明单个基因的重叠有助于小鼠的焦虑样行为模型和人类焦虑特征。当基因作为集合进行测试时,我们确实确定了小鼠基因集合与人类焦虑之间的14个显著关联,但大多数基因集合与人的焦虑表型没有显著关联。这些为数不多的显著关联表明,需要通过识别模型系统和感兴趣的特定人类表型之间“匹配”的基因集来识别和开发更可翻译的小鼠模型。我们认为,继续开发改进的行为范式和更精细的实验数据,例如来自单个神经元亚型或细胞类型特异性表达数据,可能会提高我们对焦虑症的遗传病因和潜在功能变化的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Testing associations between human anxiety and genes previously implicated by mouse anxiety models

Testing associations between human anxiety and genes previously implicated by mouse anxiety models

Testing associations between human anxiety and genes previously implicated by mouse anxiety models

Anxiety disorders are common and can be debilitating, with effective treatments remaining hampered by an incomplete understanding of the underlying genetic etiology. Improvements have been made in understanding the genetic influences on mouse behavioral models of anxiety, yet it is unclear the extent to which genes identified in these experimental systems contribute to genetic variation in human anxiety phenotypes. Leveraging new and existing large-scale human genome-wide association studies, we tested whether sets of genes previously identified in mouse anxiety-like behavior studies contribute to a range of human anxiety disorders. When tested as individual genes, 13 mouse-identified genes were associated with human anxiety phenotypes, suggesting an overlap of individual genes contributing to both mouse models of anxiety-like behaviors and human anxiety traits. When genes were tested as sets, we did identify 14 significant associations between mouse gene sets and human anxiety, but the majority of gene sets showed no significant association with human anxiety phenotypes. These few significant associations indicate a need to identify and develop more translatable mouse models by identifying sets of genes that “match” between model systems and specific human phenotypes of interest. We suggest that continuing to develop improved behavioral paradigms and finer-scale experimental data, for instance from individual neuronal subtypes or cell-type-specific expression data, is likely to improve our understanding of the genetic etiology and underlying functional changes in anxiety disorders.

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来源期刊
Genes Brain and Behavior
Genes Brain and Behavior 医学-行为科学
CiteScore
6.80
自引率
4.00%
发文量
62
审稿时长
4-8 weeks
期刊介绍: Genes, Brain and Behavior was launched in 2002 with the aim of publishing top quality research in behavioral and neural genetics in their broadest sense. The emphasis is on the analysis of the behavioral and neural phenotypes under consideration, the unifying theme being the genetic approach as a tool to increase our understanding of these phenotypes. Genes Brain and Behavior is pleased to offer the following features: 8 issues per year online submissions with first editorial decisions within 3-4 weeks and fast publication at Wiley-Blackwells High visibility through its coverage by PubMed/Medline, Current Contents and other major abstracting and indexing services Inclusion in the Wiley-Blackwell consortial license, extending readership to thousands of international libraries and institutions A large and varied editorial board comprising of international specialists.
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