R E Moreira-Júnior, R M Souza, J G de Carvalho, J P Bergamini, A L Brunialti-Godard
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引用次数: 2
摘要
在动物和人类中,LRRK2基因的改变与帕金森病和饮酒有关。此外,这些障碍与焦虑症(ADs)密切相关。因此,我们研究了LRRK2基因如何影响人类和小鼠的焦虑。我们根据PRISMA声明对LRRK2基因改变的动物或人类模型的焦虑水平进行了系统回顾。在PubMed、Scopus和Web of Science数据库中进行搜索,并在带有与ad和LRRK2相关描述符的参考文献列表中进行搜索。在62篇合格评估的文章中,包括16篇:11篇在人类身上进行,7篇在小鼠身上进行。Lrrk2 KO小鼠以及Lrrk2 G2019S、Lrrk2 R1441G和Lrrk2 R1441C变体进行了研究。五篇文章报道了与LRRK2变异相关的焦虑水平增加。两篇文章观察到焦虑水平下降,一篇关注LRRK2 G2019S,另一篇关注LRRK2 KO小鼠。其他八篇文章报道,与健康对照组相比,Lrrk2变异个体的焦虑水平没有差异。本研究探讨了LRRK2基因与焦虑之间可能存在的影响,为现有关于遗传对焦虑影响的知识增加了信息。
Possible association between the lrrk2 gene and anxiety behavior: a systematic literature review.
Alterations to the LRRK2 gene have been associated with Parkinson's disease and alcohol consumption in animals and humans. Furthermore, these disorders are strongly related to anxiety disorders (ADs). Thus, we investigated how the LRRK2 gene might influence anxiety in humans and mice. We elaborated a systematic review based on the PRISMA Statement of studies that investigated levels of anxiety in animal or human models with alterations in the LRRK2 gene. The search was conducted in the PubMed, Scopus, and Web of Science databases, and in reference lists with descriptors related to ADs and the LRRK2. From the 62 articles assessed for eligibility, 16 were included: 11 conducted in humans and seven, in mice. Lrrk2 KO mice and the LRRK2 G2019S, LRRK2 R1441G, and LRRK2 R1441C variants were addressed. Five articles reported an increase in anxiety levels concerning the LRRK2 variants. Decreased anxiety levels were observed in two articles, one focusing on the LRRK2 G2019S and the other, on the Lrrk2 KO mice. Eight other articles reported no differences in anxiety levels in individuals with Lrrk2 alterations compared to their healthy controls. This study discusses a possible influence between the LRRK2 gene and anxiety, adding information to the existing knowledge respecting the influence of genetics on anxiety.
期刊介绍:
The Journal is appropriate for papers on behavioral, biochemical, or cellular aspects of neural function, plasticity, aging or disease. In addition to analyses in the traditional genetic-model organisms, C. elegans, Drosophila, mouse and the zebrafish, the Journal encourages submission of neurogenetic investigations performed in organisms not easily amenable to experimental genetics. Such investigations might, for instance, describe behavioral differences deriving from genetic variation within a species, or report human disease studies that provide exceptional insights into biological mechanisms