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Elucidating risk mechanisms of gene–environment interactions on pediatric anxiety: integrating findings from neuroscience

机译:阐明儿童焦虑症中基因与环境相互作用的风险机制:整合神经科学的发现

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摘要

Recent findings of gene–environment interaction on child and adolescent anxiety generate interest in mechanisms through which genetic risks are expressed. Current findings from neuroscience suggest avenues for exploring putative mechanisms. Specifically recent documentations of abnormality in brain function among anxious adolescents may reflect the end-result of gene expression. In turn these inherited predispositions may increase the likelihood of psychopathology in the presence of stress. The aim of the current article is to consider putative mechanisms reflecting genetic sensitivity to the environment (G × E). Thus we review data implicating biased processing of threat information and anomalies in brain circuitry in the expression of pediatric anxiety. These data suggest that links across development among genes, brain, psychological processes, and behavior are far from established. Accordingly, the article proposes strategies for examining these links. Exploring these relationships during development is crucial, given that these early life processes may potentially shape longer-term patterns of emotional behavior, and therefore life-long trajectories of anxiety.
机译:有关儿童和青少年焦虑的基因-环境相互作用的最新发现引起了人们对表达遗传风险的机制的兴趣。神经科学的最新发现为探索推测的机制提供了途径。特别是最近有关焦虑症患者脑功能异常的文献可能反映了基因表达的最终结果。反过来,这些遗传的倾向可能会在压力下增加心理病理学的可能性。本文的目的是考虑反映遗传对环境敏感性的推定机制(G×E)。因此,我们审查了涉及小儿焦虑症表达中威胁信息和大脑回路异常处理的偏向数据。这些数据表明,基因,大脑,心理过程和行为之间的发育联系还很遥远。因此,本文提出了研究这些链接的策略。鉴于这些早期生活过程可能会影响情绪行为的长期模式,从而影响人们一生的焦虑轨迹,因此在发展过程中探索这些关系至关重要。

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