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Lack of Evidence for the Neural Noise Hypothesis in Dyslexia: Insights from EEG and 7T MRS Excitation-Inhibition Balance Biomarkers
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Poster C21 in Poster Session C, Friday, October 25, 4:30 - 6:00 pm, Great Hall 4
Agnieszka Glica1, Katarzyna Wasilewska1, Julia Jurkowska2, Jarosław Żygierewicz2, Bartosz Kossowski3, Katarzyna Jednoróg1; 1Laboratory of Language Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland, 2Faculty of Physics, University of Warsaw, Warsaw, Poland, 3Laboratory of Brain Imaging, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland
The neural noise hypothesis of dyslexia posits an imbalance between excitatory and inhibitory (E/I) brain activity as an underlying mechanism of reading difficulties, specifically suggesting increased glutamate (Glu) levels in individuals with dyslexia. Although the hypothesis was proposed seven years ago, the body of research validating its predictions remains scarce. This study provides the first direct test of the neural noise hypothesis using both indirect EEG power spectrum measures – exponent, offset, and beta power – in 120 Polish adolescents and young adults (60 with dyslexia, 60 controls) and direct Glu and GABA concentrations from magnetic resonance spectroscopy (MRS) at a 7T MRI scanner in half of the sample. Previous work has shown associations between a flatter slope of the EEG power spectrum (lower exponent) and greater dominance of excitation over inhibition, and between greater GABAergic activity and increased EEG beta power. Hence, in line with the neural noise hypothesis, we expected to find higher Glu levels, lower exponent, and lower beta power in participants with dyslexia. Our results, supported by Bayesian statistics, show no evidence for group differences in the indirect EEG measures of the E/I balance tested both at rest and during a spoken language task. Similarly, no evidence for group differences was found in the MRS-derived Glu and GABA concentrations in the individually localized language-sensitive left superior temporal cortex. Overall, our results challenge the prediction that cortical hyperexcitability is an underlying causal factor for developmental dyslexia and suggest that alternative mechanisms must be explored.
Topic Areas: Disorders: Developmental, Reading