Molecular genetic examination of rapid automatized naming and rapid alternating stimulus in Hispanic and African American youth: A multivariate approach.

Molecular genetic examination of rapid automatized naming and rapid alternating stimulus in Hispanic and African American youth: A multivariate approach.

First Author: Andrew Adams -- Yale University
Additional authors/chairs: 
Dongnhu Truong; Joan Bosson-Heenan; Jeffrey R. Gruen;
Abstract / Summary: 

Purpose: The complex genetic architecture of reading disability and co-occurring diverse cognitive impairments pose challenges for identifying novel risk genes and variants. To address this challenge, we took advantage of the high correlation between rapid automatized naming (RAN), rapid alternating stimulus (RAS) and single word reading, to identify shared genetic factors that may contribute to common biological mechanisms between RAN, RAS, and word reading.

Methods: We conducted a multivariate genome-wide association analysis to identify shared genetic factors that contribute to performance across RAN Objects, RAN Letters, and RAS Letters and Numbers in a sample of 1,331 Hispanic and African American youth that were recruited in the GRaD Study. Follow-up neuroimaging genetics analysis in the PING study and bioinformatic analysis using the Roadmap Epigenetics Project were conducted to identify potential biological mechanisms underlying RAN and RAS performance.

Results: Genome-wide significant effects across RAN Objects, RAN Letters, and RAS Letters and Numbers were observed for SNPs located on chromosome 10q23.31. Single SNP analysis also showed significant association with measures of single word reading performance. Follow-up bioinformatic analysis of this region indicate brain-specific functionality, with neuroimaging genetic analysis showing association with cortical volume in the right inferior parietal cortex—a region of the brain previously associated with numerical information and reading disability.

Conclusion: This study provides support for a novel trait locus at chromosome 10q23.31 with shared genetic effects across RAN, RAS, cortical volume, and word reading, and provides a target for future functional analysis to understand underlying biological mechanisms for reading (dis)ability.