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<p>Auditory processing abnormalities are a prominent feature of Autism Spectrum Disorder (ASD), significantly affecting sensory integration, communication, and social interaction. This review delves into the neurobiological mechanisms underlying these deficits, including structural and functional disruptions in the auditory cortex, imbalances in excitatory and inhibitory signaling, and synaptic dysfunction. Genetic contributions from mutations in CNTNAP2, SHANK3, FMR1, and FOXP2 are explored, highlighting their roles in auditory abnormalities. Animal models, such as BTBR<sup>T+tf/J</sup> mice (BTBR) and valproic acid (VPA)-exposed rodents, provide critical insights into the sensory abnormalities observed in ASD. In addition, the review discusses current pharmacological strategies and emerging interventions targeting neurotransmitter systems and synaptic plasticity. Notably, future directions are emphasized, highlighting the need for integrated pharmacological and auditory-specific therapies to enhance sensory processing and communication outcomes in ASD. Overall, this review aims to bridge the gap between basic neurobiological research and clinical application, guiding future studies and therapeutic developments in ASD-related auditory processing deficits.</p>

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Auditory processing deficits in autism spectrum disorder: mechanisms, animal models, and therapeutic directions

  • 期刊论文

  • 发表日期：

    2025年5月12日

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  • Shuyu Zheng,
  • Chen Chen

摘要

Auditory processing abnormalities are a prominent feature of Autism Spectrum Disorder (ASD), significantly affecting sensory integration, communication, and social interaction. This review delves into the neurobiological mechanisms underlying these deficits, including structural and functional disruptions in the auditory cortex, imbalances in excitatory and inhibitory signaling, and synaptic dysfunction. Genetic contributions from mutations in CNTNAP2, SHANK3, FMR1, and FOXP2 are explored, highlighting their roles in auditory abnormalities. Animal models, such as BTBRT+tf/J mice (BTBR) and valproic acid (VPA)-exposed rodents, provide critical insights into the sensory abnormalities observed in ASD. In addition, the review discusses current pharmacological strategies and emerging interventions targeting neurotransmitter systems and synaptic plasticity. Notably, future directions are emphasized, highlighting the need for integrated pharmacological and auditory-specific therapies to enhance sensory processing and communication outcomes in ASD. Overall, this review aims to bridge the gap between basic neurobiological research and clinical application, guiding future studies and therapeutic developments in ASD-related auditory processing deficits.