Behaviour genetic analyses of reading and spelling: A component processes approach
Behaviour genetic analyses of reading and spelling: A component processes approach
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DOI：
10.1080/00049530410001734847
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发表时间：
2004-09-01
影响因子：
2.7
通讯作者：
Martin, NG
中科院分区：
文献类型：
--
作者：
Bates, TC;Castles, A;Martin, NG
本文报告了一个大样本的双胞胎青少年阅读和拼写差异的遗传和环境基础。介绍了阅读的双路径级联（DRC）模型，并将其用于为阅读的基本心理功能提供内表型。然后，该模型扩展到一个互补的双路模型的拼写测试挖掘词汇和子词汇路径拼写。报告了基于DRC的表型的单变量分析。模型拟合支持高水平的加性遗传控制学习阅读（遗传率为0.73，0.71，0.61的不规则，非文字，和经常的字阅读分别），与其余的方差最好建模为独特的环境（包括测量误差），而不是家庭之间的差异。同样，在本设计的能力范围内，不支持指定性别限制遗传机制的模型，这表明两种阅读途径的基因对于两种性别是相同的，并且控制相似的方差比例。对于拼写，词汇和非词汇阅读任务的遗传力相似（h（2）分别为0.76，0.52）。未来的多元分析的价值进行了讨论，从竞争的心理模型的阅读测试预测，是需要联系和协会的研究和发展更基本的endophenotypes，以充分解决这一重要的人类行为的遗传结构。
This paper reports on the genetic and environmental bases of differences in reading and spelling in a large unselected adolescent twin sample. The dual route cascaded (DRC) model of reading is introduced and used to provide endophenotypes for the basic psychological functions underlying reading. The model is then extended to a complementary dual-route model for spelling with tests tapping lexical and sublexical routes to spelling. Univariate analyses of the DRC-based phenotypes are reported. Model fitting supported high levels of additive genetic control over learning to read (heritabilities of 0.73, 0.71, and 0.61 for irregular, nonword, and regular word reading respectively), with remaining variance being best modelled as unique environment (including measurement error) rather than differences between families. Again, within the power of the present design, models specifying sex-limited genetic mechanisms were not supported, suggesting that the genes for both routes to reading are the same for both sexes and control similar proportions of variance. For spelling, the heritabilities were similar for the tasks corresponding to lexical and nonlexical reading (h(2) = 0.76, 0.52 respectively). The value of future multivariate analyses for testing predictions from competing psychological models of reading are discussed, as is the need for linkage and association studies and for the development of more basic endophenotypes to fully resolve the genetic architecture of this important human behaviour.