Summary: Researchers report a gene associated with dyslexia may interfere with speech processing.
Source: UT Dallas.
A new study led by UT Dallas researchers shows that a gene associated with dyslexia may interfere with the processing of speech, ultimately leading to reading problems that are characteristic of the disorder.
While previous studies have tied the DCDC2 gene to dyslexia, Dr. Michael Kilgard, a neuroscientist at UT Dallas and one of the study’s co-authors, said the new findings are the first to demonstrate that the gene is required for normal auditory processing of complex speech.
According to Kilgard, there are two theories about the cause of dyslexia: a visual or memory theory, and the auditory theory. “This study puts more weight on the side of the auditory theory,” he said.
“We now have evidence that strongly suggests that people with dyslexia don’t actually hear all of the sounds they need to hear,” said Kilgard, who is the Margaret Fonde Jonsson Professor in the School of Behavioral and Brain Sciences and the associate director of the Texas Biomedical Device Center.
“If you have trouble hearing the sounds in your language, you will have trouble learning to read later,” he said. “Armed with this information about a genetic link, we may be able to determine who is at risk for reading problems before they have trouble — before they even start learning to read.”
The study, which appears in the Journal of Neuroscience, involved healthy rats that were taught a variety of speech sound discrimination tasks. When the DCDC2 gene was suppressed, the rats were virtually unable to identify specific speech sounds.
Kilgard equated the speech discrimination problems with issues experienced by children as they try to learn language skills.
He said the good news about the discovery is that individuals who have trouble distinguishing sounds could potentially recover that ability through therapy and neural training.
“Neural responses actually can be changed by training. Repetition does change those brain networks,” Kilgard said. “The more you know about genes, the more you can overcome the issues even if there is never a pill to solve the problem.”
Kilgard is known for his research that uses vagus nerve stimulation paired with training to encourage neural plasticity, which is the reorganization of neural responses in the brain. He has shown that VNS can enhance plasticity and rehabilitation in multiple animal models and in patients with stroke and tinnitus.
Kilgard said the new findings provide a new tool that could change how we look at learning disabilities.
“Instead of making assumptions about what a child can achieve in life, children who have trouble distinguishing sounds can attain great things, although it may take more effort. Instead of getting there in 20 hours it may take 100 hours,” he said.
Kilgard said certain commercial gene testing products can detect impaired genes, including DCDC2. But he said more work is needed to fully understand the link between neural processing and dyslexia.
The study was led by Dr. Tracy Centanni MS’11, PhD’13, who began her research as a UT Dallas graduate student in the School of Behavioral and Brain Sciences. She is now a postdoctoral researcher at the Massachusetts Institute of Technology. Dr. Robert Rennaker, Texas Instruments Distinguished Chair in Bioengineering, director of the Texas Biomedical Device Center and chairman of the Department of Bioengineering, was a co-author of the study, as were UT Dallas’ Andrew Sloan and Ryan Carraway, as well as a team from the University of Connecticut.
Funding: The work was supported by National Institute of Deafness and Other Communication Disorders at the National Institutes of Health.
Source: Phil Roth – UT Dallas
Image Source: This NeuroscienceNews.com image is adapted from the UT Dallas press release.
Original Research: Abstract for “Knockdown of Dyslexia-Gene Dcdc2 Interferes with Speech Sound Discrimination in Continuous Streams” by Tracy Michelle Centanni, Anne B. Booker, Fuyi Chen, Andrew M. Sloan, Ryan S. Carraway, Robert L. Rennaker, Joseph J. LoTurco, and Michael P. Kilgard in Journal of Neuroscience. Published online April 27 2016 doi:10.1523/JNEUROSCI.4202-15.2016
[cbtabs][cbtab title=”MLA”]UT Dallas. “Gene Contributes to Poor Speech Processing and Dyslexia.” NeuroscienceNews. NeuroscienceNews, 11 July 2016.
<https://neurosciencenews.com/genetics-dyslexia-speech-processing-4649/>.[/cbtab][cbtab title=”APA”]UT Dallas. (2016, July 11). Gene Contributes to Poor Speech Processing and Dyslexia. NeuroscienceNew. Retrieved July 11, 2016 from https://neurosciencenews.com/genetics-dyslexia-speech-processing-4649/[/cbtab][cbtab title=”Chicago”]UT Dallas. “Gene Contributes to Poor Speech Processing and Dyslexia.” https://neurosciencenews.com/genetics-dyslexia-speech-processing-4649/ (accessed July 11, 2016).[/cbtab][/cbtabs]
Altered proliferation and networks in neural cells derived from idiopathic autistic individuals
Dyslexia is the most common developmental language disorder and is marked by deficits in reading and phonological awareness. One theory of dyslexia suggests that the phonological awareness deficit is due to abnormal auditory processing of speech sounds. Variants in DCDC2 and several other neural migration genes are associated with dyslexia and may contribute to auditory processing deficits. In the current study, we tested the hypothesis that RNAi suppression of Dcdc2 in rats causes abnormal cortical responses to sound and impaired speech sound discrimination. In the current study, rats were subjected in utero to RNA interference targeting of the gene Dcdc2 or a scrambled sequence. Primary auditory cortex (A1) responses were acquired from 11 rats (5 with Dcdc2 RNAi; DC−) before any behavioral training. A separate group of 8 rats (3 DC−) were trained on a variety of speech sound discrimination tasks, and auditory cortex responses were acquired following training. Dcdc2 RNAi nearly eliminated the ability of rats to identify specific speech sounds from a continuous train of speech sounds but did not impair performance during discrimination of isolated speech sounds. The neural responses to speech sounds in A1 were not degraded as a function of presentation rate before training. These results suggest that A1 is not directly involved in the impaired speech discrimination caused by Dcdc2 RNAi. This result contrasts earlier results using Kiaa0319 RNAi and suggests that different dyslexia genes may cause different deficits in the speech processing circuitry, which may explain differential responses to therapy.
SIGNIFICANCE STATEMENT Although dyslexia is diagnosed through reading difficulty, there is a great deal of variation in the phenotypes of these individuals. The underlying neural and genetic mechanisms causing these differences are still widely debated. In the current study, we demonstrate that suppression of a candidate-dyslexia gene causes deficits on tasks of rapid stimulus processing. These animals also exhibited abnormal neural plasticity after training, which may be a mechanism for why some children with dyslexia do not respond to intervention. These results are in stark contrast to our previous work with a different candidate gene, which caused a different set of deficits. Our results shed some light on possible neural and genetic mechanisms causing heterogeneity in the dyslexic population.
“Knockdown of Dyslexia-Gene Dcdc2 Interferes with Speech Sound Discrimination in Continuous Streams” by Tracy Michelle Centanni, Anne B. Booker, Fuyi Chen, Andrew M. Sloan, Ryan S. Carraway, Robert L. Rennaker, Joseph J. LoTurco, and Michael P. Kilgard in Journal of Neuroscience. Published online April 27 2016 doi:10.1523/JNEUROSCI.4202-15.2016