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          <dc:identifier>https://hdl.handle.net/2286/R.2.N.201300</dc:identifier>
                  <dc:rights>http://rightsstatements.org/vocab/InC/1.0/</dc:rights>
          <dc:rights>All Rights Reserved</dc:rights>
                  <dc:date>2025</dc:date>
          <dc:date>2027-05-01T17:45:47</dc:date>
                  <dc:format>144 pages</dc:format>
                  <dc:type>Doctoral Dissertation</dc:type>
          <dc:type>Academic theses</dc:type>
                  <dc:language>en</dc:language>
                  <dc:contributor>Kim, Yookyung</dc:contributor>
          <dc:contributor>Peter, Beate</dc:contributor>
          <dc:contributor>Daliri, Ayoub</dc:contributor>
          <dc:contributor>Klein-Seetharaman, Judith</dc:contributor>
          <dc:contributor>Liu, Li</dc:contributor>
          <dc:contributor>Gray, Shelley</dc:contributor>
          <dc:contributor>Arizona State University</dc:contributor>
                  <dc:description>Partial requirement for: Ph.D., Arizona State University, 2025</dc:description>
          <dc:description>Field of study: Speech and Hearing Science</dc:description>
          <dc:description>Dyslexia is a neurodevelopmental disorder characterized by difficulties with accurate and/or fluent recognition, spelling, and decoding of words, primarily attributed to deficits in phonological processing. This dissertation explores gene-brain-behavior relationships underlying dyslexia. A special focus is on sensory gating, a neural mechanism for filtering out redundant auditory stimuli, as a robust neurophysiological endophenotype linked to dyslexia’s core deficits. Employing electrophysiological assessments, including event-related potential (ERP) components, mismatch negativity (MMN), and auditory steady-state response (ASSR), this study identified significantly reduced N1 gating magnitudes in individuals with dyslexia compared to controls. Importantly, gating magnitude was correlated with phonemic decoding efficiency (PDE), word identification (WID), and rapid automatized naming (RAN), supporting the neural noise hypothesis. A distinct dyslexia subgroup, identified through cluster analysis, demonstrated pronounced gating impairments coupled with specific genetic variants and poorer behavioral performance on phonological processing and integration of temporal information, underscoring dyslexia&#039;s phenotypic variability and the significance of sensory gating deficits. Genetic analyses further revealed associations between sensory gating and genes such as CNTNAP2, TDRD5, and GRIK4, with known roles in neural excitability, synaptic signaling, and neuronal connectivity. Integrated bioinformatics using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and Gene Ontology (GO) analyses highlighted biological pathways relevant to neurodevelopment and neurophysiology, including synaptic organization, neuronal migration, ion transport, and intracellular signaling, shedding light on the genetic basis of sensory gating deficits. These findings collectively offer evidence that dyslexia may arise from increased neural variability or &quot;neural noise,&quot; driven by genetic variants impacting neural excitability and synaptic stability. Such insights pave the way for early, genetically informed identification of at-risk individuals and highlight targeted intervention strategies aimed at reducing neural noise and improving sensory gating, potentially mitigating dyslexia’s adverse effects on literacy development.

</dc:description>
                  <dc:subject>Speech therapy</dc:subject>
          <dc:subject>Genetics</dc:subject>
          <dc:subject>Neurosciences</dc:subject>
                  <dc:title>A Multifaceted Account of Auditory Encoding in Dyslexia: Evidence from Cortical   Electroencephalography, Genetic Influences, and Clinical Subphenotype</dc:title></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>
