Congenital amusia is a lifelong disorder that compromises the normal development of musical abilities in 1.5–4% of the general population. There is a substantial genetic contribution to congenital amusia, and it bears similarities to neurodevelopmental disorders of language. Here, we examine the extent to which variants in the forkhead box P2 gene (FOXP2)—the first gene to be identified as causal in developmental speech deficits—are associated with the amusic trait. Using a cohort of 49 individuals with amusia, of which 27 were unrelated, the role of FOXP2 variants in amusia was evaluated. Fourteen variants were examined in the cohort. None segregated with the amusic trait among participants for whom family information was available; nor were they predicted to be deleterious to protein function. Thus, variants in FOXP2 are not likely to cause amusia. Implications for ongoing debates about the distinction between musicality and language are discussed.

中文翻译：

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FOXP2（一种与语言障碍有关的基因）编码区的变异是否会带来先天性失乐症的风险？

先天性失乐症是一种终生疾病，会影响 1.5-4% 的普通人群音乐能力的正常发展。先天性失乐症有很大的遗传因素，它与语言的神经发育障碍有相似之处。在这里，我们研究了叉头框 P2 基因 ( FOXP2)中的变异在多大程度上与音乐特征相关——第一个被确定为发育性言语缺陷的因果基因。使用一组 49 名患有失乐症的个体，其中 27 名无关，FOXP2的作用评估了 amusia 中的变体。在队列中检查了 14 个变体。在可获得家庭信息的参与者中，没有人与音乐特征隔离；也没有预测它们对蛋白质功能有害。因此，FOXP2中的变体不太可能导致失乐症。讨论了关于音乐性和语言之间的区别的持续辩论的影响。