Multi-site Study of Dyslexia

项目总结/摘要 [The一项拟议中的研究验证了一个假设，即非典型的大脑对称性会增加 阅读障碍通过阅读障碍相关基因的表达，已知调节大脑发育。而 早期有一些有希望的发现将颞平面对称性与阅读障碍联系起来， 小样本量，不一致的测量方法，以及不同的行为和遗传特征， 受试者的结果不一致。[Here我们检查了颞平面和其他大脑对称性 与诵读困难有关]。我们通过使用现有的大型数据集来解决以前研究的局限性。 遗传、神经成像和行为数据，以及我们目前开发的多位点方法， 资助期间，使解决诵读困难的假设与大型多站点数据集。我们有 证明了处理缺失数据、不同图像采集和行为异质性的能力 阅读障碍的样本是受抽样方法的影响。[具体目标1是检验以下假设： 对于特定的阅读残疾概况，观察到非典型的大脑不对称，这在理论上和 以遗传学为基础，并映射到不同的遗传风险。具体目标2是检查 阅读障碍的特定遗传风险变异影响大脑不对称的发展。具体目标3 是开发基于云的基础设施，为研究人员提供用于研究的辅助数据 并复制我们的发现（例如，与诵读困难相关的大脑不对称测量）。结果将提供 由于我们的大数据集和合作， 方法，为阅读障碍提供行为神经遗传学解释，并为研究提供资源 促进我们对阅读障碍和其他发育障碍的理解。

PROJECT SUMMARY/ABSTRACT [The proposed research tests the hypothesis that atypical cerebral symmetries increase the risk for dyslexia through the expression of dyslexia-related genes that are known to regulate brain development.] While there were early promising findings linking planum temporale symmetry to dyslexia, study limitations due to small sample size, inconsistent measurement methods, and varied behavioral and genetic profiles of the subjects produced inconsistent results. [Here we examine planum temporale and other cerebral symmetries associated with dyslexia]. We address the limitations of previous studies by using a large dataset of existing genetic, neuroimaging, and behavioral data, as well as multi-site methods that we developed in the current funding period that make it possible to address dyslexia hypotheses with large multisite datasets. We have demonstrated the ability to deal with missing data, varied image acquisitions, and the behavioral heterogeneity of dyslexia samples that is influenced by sampling approaches. [Specific Aim 1 is to test the hypothesis that atypical cerebral asymmetries are observed for specific reading disability profiles, which are theoretically and empirically-grounded and map to different genetic risks. Specific Aim 2 is to examine the degree to which specific genetic risk variants for dyslexia influence the development of cerebral asymmetries. Specific Aim 3 is to develop the cloud-based infrastructure to provide investigators with secondary data for use in their studies and to replicate our findings (e.g., cerebral asymmetry measures related to dyslexia). The results will provide a consensus on the cerebral asymmetry hypothesis for dyslexia because of our large dataset and collaborative approach, provide behavioral neurogenetic explanations for dyslexia, and provide resources to the research community to advance our understanding of dyslexia and other developmental disorders.]