Development of biomarkers in deciduous teeth of children with FASD that predict neurobehavioral performance

项目总结/摘要 产前酒精暴露后遗症，统称为胎儿酒精谱系障碍（FASD），是多种多样的 在10%的小学生中存在。它们会影响认知功能， 身体和精神健康，是一个重大的公共卫生问题。及时和适当的治疗 可以积极影响儿童的发展轨迹，防止继发性残疾。在大多数 在某些情况下，FASD的诊断需要产前酒精暴露的文件。产前酒精的生物标志物 暴露将允许在无法获得母亲自我报告的情况下诊断儿童。预防和治疗 这些努力将受益于能够非侵入性地评估子宫内膜异位症的程度和妊娠时间的生物标志物， 暴露。此外，对FASD病因学的研究将受益于这些标志物和对FASD的改良。 我们目前对机制的理解我们建议开发牙齿组织中的生物标志物， 测量暴露，允许记录自然脱落的落叶（婴儿）的产前酒精暴露 牙齿和产前暴露与神经行为缺陷的联系。我们将优化我们的技术， 能够检测到第二和第三个月的暴露。我们将测试我们的新型生物标志物 预测神经行为表现。在梳理暴露和结果之间的联系时，我们的研究 从特征良好的CIFASD队列中获益，其中持续收集已有数据， 与新的生物标志物发现一起访问和分析。本研究将提供初步数据， R 01或U 01应用程序，用于合并CIFASD数据阵列中存在的附加结果数据，例如 作为神经成像，评估共同暴露的影响，并进一步校准和提高我们的预测能力 在更大的样本中。

PROJECT SUMMARY/ ABSTRACT Prenatal alcohol exposure sequelae, collectively termed Fetal Alcohol Spectrum Disorders (FASD), are varied and present in as many as 10% of elementary school children. They affect cognitive functioning, as well as physical and mental health, and represent a significant public health issue. Timely and appropriate treatment can positively impact a child’s developmental trajectory and prevent secondary disabilities. In the majority of cases, diagnosis of FASD requires documentation of prenatal alcohol exposure. A biomarker of prenatal alcohol exposure would allow diagnosis of children where maternal self-report is unavailable. Prevention and treatment efforts would benefit from biomarkers able to noninvasively assess the magnitude and gestational time of exposures. Additionally, research into the etiology of FASD would benefit from such markers and the refining of our current understanding of mechanisms. We propose to develop biomarkers in dental tissue to quantitatively measure exposures, allowing the documentation of prenatal alcohol exposure in naturally shed deciduous (baby) teeth and the linking of prenatal exposures to neurobehavioral deficits. We will optimize our techniques to be able to detect exposures by month of second and third trimester. We will test whether our novel biomarkers predict neurobehavioral performance. In teasing out associations among exposures and outcomes, our study benefits from the well-characterized CIFASD cohort where consistently gathered, already existing data may be accessed and analyzed in conjunction with novel biomarker findings. This study will provide preliminary data for an R01 or U01 application to incorporate additional outcome data existing within the array of CIFASD data, such as neuroimaging, assess the effects of co-exposures, and further calibrate and improve our predictive capacity within the larger sample.