自闭症生物化学

邓文龙

自闭症生物化学
（自闭症科普知识）
自闭症生物化学 ： 自闭症谱系障碍（ASD）是一种复杂的神经发育障碍，其生物化学机制涉及遗传、环境和神经生物学等多种因素。研究表明，ASD患者的致病基因可能编码突触功能相关的蛋白质，如细胞粘附分子、突触囊泡循环蛋白和离子转运蛋白等，这些基因的突变可能导致神经元之间的信息传递异常，从而引发自闭症症状。  
此外，表观遗传学研究也显示，环境因素可能通过影响基因表达而增加ASD的风险。例如，孕期接触某些化学物质，如三氯生，可能通过抑制视黄酸合成，影响胎儿大脑发育，增加后代患自闭症的风险。  
神经递质系统的异常也是ASD研究的重点之一。研究发现，ASD患者的GABA（γ-氨基丁酸）信号传导可能存在异常，影响神经元的兴奋性和平衡，进而导致自闭症相关症状。  
针对这些生物化学机制的研究，为ASD的潜在治疗策略提供了新的思路。例如，补充视黄酸或调节GABA受体功能的药物可能有助于缓解自闭症症状。然而，由于ASD的异质性和复杂性，仍需更多研究以全面理解其生物化学机制，并开发有效的干预措施。



( Software translation )   Autism biochemistry: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder with biochemical mechanisms involving multiple factors such as genetics, environment, and neurobiology. Studies have shown that the causative genes of ASD may encode proteins related to synaptic function, such as cell adhesion molecules, synaptic vesicle cycle proteins, and ion transporters. Mutations in these genes may lead to abnormal information transmission between neurons, resulting in autism symptoms.
In addition, epigenetic studies have also shown that environmental factors may increase the risk of ASD by affecting gene expression. For example, exposure to certain chemicals during pregnancy, such as triclosan, may affect fetal brain development by inhibiting retinoic acid synthesis, increasing the risk of autism in offspring.
Abnormalities in the neurotransmitter system are also one of the focuses of ASD research. Studies have found that the GABA (gamma-aminobutyric acid) signal transduction in ASD patients may be abnormal, which affects the excitability and balance of neurons, leading to autism-related symptoms.
Research on these biochemical mechanisms provides new ideas for potential treatment strategies for ASD. For example, supplements of retinoic acid or drugs that regulate the function of GABA receptors may help alleviate symptoms of autism. However, due to the heterogeneity and complexity of ASD, more research is needed to comprehensively understand its biochemical mechanisms and develop effective interventions.