Prenatal Neurogenesis in Autism Spectrum Disorders.
Prenatal Neurogenesis in Autism Spectrum Disorders.
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DOI：
10.3389/fchem.2016.00012
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发表时间：
2016
影响因子：
5.5
通讯作者：
Zarbalis KS
中科院分区：
文献类型：
--
作者：
Kaushik G;Zarbalis KS
越来越多的文献描述了令人信服的证据，表明自闭症谱系中的一部分幼儿显示出异常的大脑发育轨迹。在这些病例中，出生时正常的大脑大小之后会有一段时间的异常生长，与未受影响的对照组相比，通常在儿童后期开始出现倒退。最近的研究表明，前额叶皮质神经元的数量异常增加，这表明自闭症患者的大脑体积增加是由过量的神经元产生驱动的。此外，一些受影响的儿童表现出皮质投射神经元的片状异常板层定位。由于皮质投射神经元的数量及其在发育中的皮质内的正确分层都需要神经前体细胞不受干扰地增殖，因此神经前体细胞似乎位于与早期脑过度生长相关的自闭症病理的中心。因此，与脑增大相关的自闭症谱系障碍应被视为早期胚胎起源的出生缺陷，对其早期诊断、预防策略和治疗干预具有深远的影响。
An ever-increasing body of literature describes compelling evidence that a subset of young children on the autism spectrum show abnormal cerebral growth trajectories. In these cases, normal cerebral size at birth is followed by a period of abnormal growth and starting in late childhood often by regression compared to unaffected controls. Recent work has demonstrated an abnormal increase in the number of neurons of the prefrontal cortex suggesting that cerebral size increase in autism is driven by excess neuronal production. In addition, some affected children display patches of abnormal laminar positioning of cortical projection neurons. As both cortical projection neuron numbers and their correct layering within the developing cortex requires the undisturbed proliferation of neural progenitors, it appears that neural progenitors lie in the center of the autism pathology associated with early brain overgrowth. Consequently, autism spectrum disorders associated with cerebral enlargement should be viewed as birth defects of an early embryonic origin with profound implications for their early diagnosis, preventive strategies, and therapeutic intervention.