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Auditory prediction and neural synchronization in dyslexia: Individual variability in mismatch negativity and auditory steady-state response linked to behavioral and genetic profiles

Poster Session E, Sunday, September 14, 11:00 am - 12:30 pm, Field House
This poster is part of the Sandbox Series.

Yookyung Kim1, Beate Peter; 1Arizona State University

Developmental dyslexia is a complex neurodevelopmental disorder characterized by persistent difficulties in fluent and accurate word recognition and reading. While group-level deficits in phonological and auditory processing are well-documented, fewer studies have examined intra-individual variability in neural processing that may underlie distinct neurobiological subtypes of dyslexia. This study investigated whether auditory evoked potentials, specifically mismatch negativity (MMN) and auditory steady-state responses (ASSRs), reveal distinct neurobiological profiles among individuals with dyslexia and whether these profiles relate to individual differences in behavioral performance and genetic variation. Based on allophonic perception and temporal sampling theory, high-density EEG recordings were collected from 27 adults (dyslexia: n = 10; control: n = 17; mean age (SD) = 20.10 (1.28) years). MMN was elicited using an oddball paradigm with the English vowel /æ/ as standard and its allophone as deviant stimuli. Difference waveforms (deviant minus standard) were averaged across 19 frontocentral electrodes. ASSRs were elicited using amplitude-modulated white noise at 2 Hz, 20 Hz, and 40 Hz. Spectral amplitude at each frequency was extracted via Fast Fourier Transform (FFT), and z-scores normalization was applied to standardize target frequencies relative to background EEG activity at 19 frontocentral electrodes. Behavioral assessments included standardized measures of phonological processing, verbal working memory, rapid automatized naming, and word and nonword reading. Repeated measures ANOVA was used to evaluate group difference and condition effects. Bonferroni correction was applied for post hoc comparisons. Correlation coefficients analyses were calculated to assess the associations between EEG indices and behavioral scores. For each participant, trial-level variabilities in MMN and ASSR responses are calculated using intra-individual SD across trials. Whole-exome sequencing (WES) was conducted on all participants. Variants were filtered based on allele frequency, predicted pathogenicity (e.g., CADD scores), and inheritance patterns. All variants were visually validated suing the Integrated Genome Viewer (IGV 1.3.) Candidate genes were categorized into high-confidence (HC) and low-confidence (LC) sets based on the American College of Medical Genetics and Genomics (ACMG) guidelines. Visual inspection and z-score distributions showed substantial intra- and inter-individual variability in MMN amplitude and ASSR amplitudes. While some participants with dyslexia demonstrated attenuated responses, consistent with impaired auditory prediction or synchronization, others exhibited intact or even enhanced responses, indicating dissociable auditory profiles not captured by group-level analyses. Correlation patterns suggested that heightened auditory change detection was associated with weaker phonological awareness and verbal working memory, whereas reduced neural entrainment was linked to slower naming and word reading fluency. Preliminary genetic findings indicated that these neural phenotypes may correspond to distinct sets of gene variants involved in synaptic signaling and neural hyperexcitability. Further variant analyses will investigate association between EEG-derived subgroups and genetic variants implicated in predictive coding, synaptic plasticity, GABAergic signaling, and cortical oscillatory regulation. These findings support the presence of neurobiological subtypes within dyslexia and MMN and ASSR as complementary markers of auditory processing differences. By integrating EEG, behavioral, and genetic data, this study provides a multidimensional understanding of dyslexia and supports efforts toward biologically informed classification and intervention strategies.

Topic Areas: Disorders: Developmental, Genetics

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