Are Molecules Involved in Neuritogenesis and Axon Guidance Related to Autism Pathogenesis?
Are Molecules Involved in Neuritogenesis and Axon Guidance Related to Autism Pathogenesis?
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DOI：
10.1007/s12017-015-8357-7
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发表时间：
2015-09-01
影响因子：
3.5
通讯作者：
Ostatnikova, Daniela
中科院分区：
文献类型：
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作者：
Bakos, Jan;Bacova, Zuzana;Ostatnikova, Daniela
自闭症谱系障碍是一种异质性疾病，许多基因表达的变化试图解释潜在的分子和病理生理原因。与细胞骨架重排、神经发生、轴突和树突延长相关的脑发育和连接异常可能代表或参与了自闭症病理的结构基础。Sit/Robo信号调节与轴突和树突分支相关的细胞骨架重构。其信号通路的组成部分(ABL和CDC42)被怀疑是正常发育改变的分子基础。本综述描述了神经发生的最重要的机制，轴突的路径发现和GTP酶在轴突生长中的作用，特别是与自闭症谱系障碍相关的改变。在分析公开的基因芯片数据的基础上，对自闭症的潜在生物标志物进行了讨论。
Autism spectrum disorder is a heterogeneous disease, and numerous alterations of gene expression come into play to attempt to explain potential molecular and pathophysiological causes. Abnormalities of brain development and connectivity associated with alterations in cytoskeletal rearrangement, neuritogenesis and elongation of axons and dendrites might represent or contribute to the structural basis of autism pathology. Slit/Robo signaling regulates cytoskeletal remodeling related to axonal and dendritic branching. Components of its signaling pathway (ABL and Cdc42) are suspected to be molecular bases of alterations of normal development. The present review describes the most important mechanisms underlying neuritogenesis, axon pathfinding and the role of GTPases in neurite outgrowth, with special emphasis on alterations associated with autism spectrum disorders. On the basis of analysis of publicly available microarray data, potential biomarkers of autism are discussed.