Haskins Laboratories, New Haven, Connecticut 06511, Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, Connecticut 06520-8042, Department of Psychology, University of Connecticut, Storrs, Connecticut 06269-1020, Department of Psychiatry, University of California San Francisco, San Francisco, California 94143-0984, Yale University Child Study Center, New Haven, Connecticut 06520, Department of Communication Disorders, Southern Connecticut State University, New Haven, Connecticut 06515, and Department of Psychology, University of Wisconsin Madison, Madison, Wisconsin 53706-1611.
J Neurosci. 2014 Mar 12;34(11):4082-9. doi: 10.1523/JNEUROSCI.3907-13.2014.
Reading disability is a brain-based difficulty in acquiring fluent reading skills that affects significant numbers of children. Although neuroanatomical and neurofunctional networks involved in typical and atypical reading are increasingly well characterized, the underlying neurochemical bases of individual differences in reading development are virtually unknown. The current study is the first to examine neurochemistry in children during the critical period in which the neurocircuits that support skilled reading are still developing. In a longitudinal pediatric sample of emergent readers whose reading indicators range on a continuum from impaired to superior, we examined the relationship between individual differences in reading and reading-related skills and concentrations of neurometabolites measured using magnetic resonance spectroscopy. Both continuous and group analyses revealed that choline and glutamate concentrations were negatively correlated with reading and related linguistic measures in phonology and vocabulary (such that higher concentrations were associated with poorer performance). Correlations with behavioral scores obtained 24 months later reveal stability for the relationship between glutamate and reading performance. Implications for neurodevelopmental models of reading and reading disability are discussed, including possible links of choline and glutamate to white matter anomalies and hyperexcitability. These findings point to new directions for research on gene-brain-behavior pathways in human studies of reading disability.
阅读障碍是一种大脑获取流畅阅读技能的障碍,影响了大量儿童。尽管典型和非典型阅读所涉及的神经解剖学和神经功能网络越来越得到很好的描述,但阅读发展个体差异的潜在神经化学基础实际上是未知的。本研究首次在支持熟练阅读的神经回路仍在发育的关键时期检查儿童的神经化学。在一个具有阅读指标从受损到优秀的新兴阅读者的纵向儿科样本中,我们研究了个体差异与使用磁共振波谱测量的神经代谢物浓度之间的关系,这些个体差异与阅读和与阅读相关的技能有关。连续和组分析都表明,胆碱和谷氨酸浓度与阅读和音韵学、词汇学等相关语言测量呈负相关(即浓度越高,表现越差)。与 24 个月后获得的行为评分的相关性表明,谷氨酸与阅读表现之间的关系具有稳定性。讨论了阅读和阅读障碍的神经发育模型的含义,包括胆碱和谷氨酸与白质异常和过度兴奋的可能联系。这些发现为阅读障碍的人类研究中的基因-大脑-行为途径的研究指明了新的方向。