Research Progress on the Relationship between Peripheral Somatosensory Neurons and Autism Spectrum Disorder

Abstract

The incidence of autism spectrum disorder (ASD) is increasing year by year worldwide and has become a global public health problem. Many studies showed that there was a close relationship between peripheral somatosensory neuron dysfunction and the pathogenesis of ASD. This article summarizes the research from domestic and foreign of the relationship between peripheral somatosensory neurons and autism spectrum disorder at home and abroad, mainly from the relationship between somatosensory neuron function and human growth and development, somatosensory disorders, the main influencing factors, and the shortcomings and prospects of research. Peripheral somatosensory neurons are the primary processing centers in somatosensory neural pathways and important information transmission hubs, which are essential for the formation of somatosensory perception; their information transmission with the brain has an important impact on brain development, the development of various complex behaviors and emotions. The influencing factors include genetic and environmental factors, of which genetic factors include γ-aminobutyric acid type A receptor subunit β3 gene mutation, methylated CpG binding protein 2 gene loss or mutation, SHANK3 gene mutation, Fmr1 gene deletion, Cntnap2 gene deletion; environmental factors such as infection, drugs, stress, and obesity. Peripheral somatosensory neurons are important dysfunction sites in the sensory disorder phenotype. Targeting peripheral somatosensory neurons may provide new strategies for somatosensory abnormalities and ASD treatment. However, due to the diversity of clinical manifestations of ASD, differences in different pathogenic genes and pathogenesis, and the high diversity of sensory interneurons in the spinal dorsal horn, the next step still needs to be in-depth study on the application of peripheral somatosensory neurons in ASD, and further clarify its internal mechanism.