Department of Pathology and Laboratory Medicine, University of California at DavisSacramento, CA, USA; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for ChildrenSacramento, CA, USA.
Front Chem. 2016 Mar 15;4:12. doi: 10.3389/fchem.2016.00012. eCollection 2016.
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.
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表现出异常的大脑生长轨迹。在这些情况下,出生时正常的大脑大小之后是一段异常的生长时期,与未受影响的对照组相比,通常从儿童晚期开始出现退行。最近的研究表明,前额叶皮层的神经元数量异常增加,这表明自闭症中大脑大小的增加是由神经元过度产生驱动的。此外,一些受影响的儿童表现出皮质投射神经元异常分层定位的斑块。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祖细胞不受干扰的增殖,因此神经祖细胞似乎处于与早期大脑过度生长相关的自闭症病理的中心。因此,与大脑扩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,这对其早期诊断、预防策略和治疗干预具有深远的意义。