Poornimai Abirami G P, Radhakrishnan Risna Kanjirassery, Johnson Esther, Roshan Syed Aasish, Yesudhas Ajisha, Parveen Suhadha, Biswas Abir, Ravichandran Vijaya Roobini, Muthuswamy Anusuyadevi, Kandasamy Mahesh
School of Life Sciences, Bharathidasan University, Tiruchirappalli, Tamil Nadu, India.
Laboratory of Stem Cells and Neuroregeneration, Department of Animal Science, School of Life Sciences, Bharathidasan University, Tiruchirappalli, Tamil Nadu, India.
Adv Neurobiol. 2020;24:207-222. doi: 10.1007/978-3-030-30402-7_8.
Autism spectrum disorder (ASD) encompasses a cluster of neurodevelopmental and genetic disorders that has been characterized mainly by social withdrawal, repetitive behavior, restricted interests, and deficits in language processing mainly in children. ASD has been known to severely impair behavioral patterns and cognitive functions including learning and memory due to defects in neuroplasticity. The biology of the ASD appears to be highly complex and heterogeneous, and thus, finding a therapeutic target for autism remains obscure. There has been no complete prevention or disease-modifying cure for this disorder. Recently, individuals with autism have been characterized by reactive neurogenesis, obstructions in axonal growth, heterotopia, resulting from dysplasia of neuroblasts in different brain regions. Therefore, it can be assumed that the aforementioned neuropathological correlates seen in the autistic individuals might originate from the defects mainly in the regulation of neuroblasts in the developing as well as adult brain. Nutrient deficiencies during early brain development and intake of certain allergic foods have been proposed as main reasons for the development of ASD. However, the integrated understanding of neurodevelopment and functional aspects of neuroplasticity working through neurogenesis in ASD is highly limited. Moreover, neurogenesis at the level of neuroblasts can be regulated by nutrition. Hence, defects in neuroblastosis underlying the severity of autism potentially could be rectified by appropriate implementation of nutraceuticals.
自闭症谱系障碍(ASD)涵盖一系列神经发育和遗传性疾病,主要特征为社交退缩、重复行为、兴趣受限以及主要在儿童中出现的语言处理缺陷。由于神经可塑性缺陷,ASD已知会严重损害行为模式和认知功能,包括学习和记忆。ASD的生物学机制似乎高度复杂且具有异质性,因此,寻找自闭症的治疗靶点仍然不明朗。对于这种疾病,目前尚无完全预防或改变疾病进程的治愈方法。最近,自闭症患者的特征表现为反应性神经发生、轴突生长受阻、异位,这是由不同脑区神经母细胞发育异常导致的。因此,可以推测自闭症个体中上述神经病理学关联可能主要源于发育中和成人大脑中神经母细胞调节的缺陷。大脑早期发育期间的营养缺乏以及某些过敏性食物的摄入被认为是ASD发病的主要原因。然而,对于通过神经发生在ASD中发挥作用的神经发育和神经可塑性功能方面的综合理解非常有限。此外,神经母细胞水平的神经发生可受营养调节。因此,通过适当使用营养保健品有可能纠正自闭症严重程度背后的神经母细胞形成缺陷。