Galvez-Contreras Alma Y, Zarate-Lopez David, Torres-Chavez Ana L, Gonzalez-Perez Oscar
Department of Neuroscience, Centro Universitario de Ciencias de la Salud, University of Guadalajara, Guadalajara 44340, Mexico.
Laboratory of Neuroscience, School of Psychology, University of Colima, Colima 28040, Mexico.
Brain Sci. 2020 Dec 8;10(12):951. doi: 10.3390/brainsci10120951.
Autism Spectrum Disorder (ASD) is an early neurodevelopmental disorder that involves deficits in interpersonal communication, social interaction, and repetitive behaviors. Although ASD pathophysiology is still uncertain, alterations in the abnormal development of the frontal lobe, limbic areas, and putamen generate an imbalance between inhibition and excitation of neuronal activity. Interestingly, recent findings suggest that a disruption in neuronal connectivity is associated with neural alterations in white matter production and myelination in diverse brain regions of patients with ASD. This review is aimed to summarize the most recent evidence that supports the notion that abnormalities in the oligodendrocyte generation and axonal myelination in specific brain regions are involved in the pathophysiology of ASD. Fundamental molecular mediators of these pathological processes are also examined. Determining the role of alterations in oligodendrogenesis and myelination is a fundamental step to understand the pathophysiology of ASD and identify possible therapeutic targets.
自闭症谱系障碍(ASD)是一种早期神经发育障碍,涉及人际沟通、社交互动和重复行为方面的缺陷。尽管ASD的病理生理学仍不确定,但额叶、边缘区域和壳核异常发育的改变会导致神经元活动的抑制和兴奋之间失衡。有趣的是,最近的研究结果表明,神经元连接中断与ASD患者不同脑区白质生成和髓鞘形成的神经改变有关。本综述旨在总结最新证据,支持特定脑区少突胶质细胞生成和轴突髓鞘形成异常参与ASD病理生理学这一观点。还研究了这些病理过程的基本分子介质。确定少突胶质细胞生成和髓鞘形成改变的作用是理解ASD病理生理学和确定可能治疗靶点的基本步骤。