少突神经胶质细胞相关自闭症谱系障碍致病机制的研究进展  

Advance in pathogenesis of oligodendrocytes-associated autism spectrum disorder

作　　者：周奕杨 傅启华[1] Zhou Yiyang;Fu Qihua(Division of Birth Defects,Institute of Translational Medicine,Shanghai Children′s Medical Center,Shanghai Jiao Tong University School of Medicine,Shanghai 200127,China)

机构地区：[1]上海交通大学医学院附属上海儿童医学中心儿科转化医学研究所出生缺陷研究室,上海200127

出　　处：《中华预防医学杂志》2022年第9期1232-1237,共6页Chinese Journal of Preventive Medicine

基　　金：上海市儿科临床分子诊断重点实验室研究项目(20dz2260900)。

摘　　要：自闭症谱系障碍(ASD)是一类危害严重的儿童神经发育障碍, 具有早期确诊难、病程时间长、损伤不可逆以及难以完全治愈等特点, 给患者、家庭和社会带来沉重的负担。近年来的研究表明, ASD的形成机制与少突神经胶质细胞系的分化、增殖及凋亡失调所导致的髓鞘形成异常关联密切。本文将阐述少突神经胶质细胞系细胞在髓鞘形成方面的作用及其分化、增殖、凋亡异常导致ASD发生的机制。少突神经胶质细胞在神经发育中发挥重要作用, 其异常是ASD重要致病机制之一。阐明其在ASD发生发展中的作用与机制, 对ASD等神经发育疾病精准防控具有积极的指导意义。Autism spectrum disorder(ASD)is a serious neurodevelopmental impairment of children.Because of its difficulty of early diagnosis,length of disease course,irreversible injury and slim chance of curability,it brings heavy burdens to patients,their families and the whole society.Recent studies have shown that the pathogenic mechanism of ASD is closely related to the abnormal myelination caused by the imbalance of differentiation,proliferation and apoptosis of oligodendroglial lineage cells.This article will review on the role of oligodendroglial lineage cells in myelination and the mechanisms of ASD caused by improper differentiation,proliferation and apoptosis of oligodendroglial lineage cells,according to advanced researches.Oligodendrocytes play vital roles in neurodevelopment,and the defect in these cells has been recognized as one of the key pathogenic mechanisms leading to ASD.Elucidating the effects and disciplines which oligodendrocytes exert on the occurrence and development of ASD would provide guidance for precise prevention and control of neurodevelopmental disorders such as ASD.

关 键 词：自闭症谱系障碍 神经发育 少突神经胶质细胞 少突神经胶质前体细胞 髓鞘 

分 类 号：R749.94[医药卫生—神经病学与精神病学]