Council for Nutritional and Environmental Medicine (CONEM), Toften 24, 8610, Mo i Rana, Norway.
Research on Children with Special Needs Department, National Research Centre, Giza, Egypt.
Mol Neurobiol. 2020 May;57(5):2314-2332. doi: 10.1007/s12035-019-01742-2. Epub 2020 Feb 5.
According to the United States Centers for Disease Control and Prevention (CDC), as of July 11, 2016, the reported average incidence of children diagnosed with an autism spectrum disorder (ASD) was 1 in 68 (1.46%) among 8-year-old children born in 2004 and living within the 11 monitoring sites' surveillance areas in the United States of America (USA) in 2012. ASD is a multifaceted neurodevelopmental disorder that is also considered a hidden disability, as, for the most part; there are no apparent morphological differences between children with ASD and typically developing children. ASD is diagnosed based upon a triad of features including impairment in socialization, impairment in language, and repetitive and stereotypic behaviors. The increasing incidence of ASD in the pediatric population and the lack of successful curative therapies make ASD one of the most challenging disorders for medicine. ASD neurobiology is thought to be associated with oxidative stress, as shown by increased levels of reactive oxygen species and increased lipid peroxidation, as well as an increase in other indicators of oxidative stress. Children with ASD diagnosis are considered more vulnerable to oxidative stress because of their imbalance in intracellular and extracellular glutathione levels and decreased glutathione reserve capacity. Several studies have suggested that the redox imbalance and oxidative stress are integral parts of ASD pathophysiology. As such, early assessment and treatment of antioxidant status may result in a better prognosis as it could decrease the oxidative stress in the brain before it can induce more irreversible brain damage. In this review, many aspects of the role of oxidative stress in ASD are discussed, taking into account that the process of oxidative stress may be a target for therapeutic interventions.
根据美国疾病控制与预防中心(CDC)的数据,截至 2016 年 7 月 11 日,在 2004 年出生并居住在美国 11 个监测点监测区域内的 8 岁儿童中,报告的自闭症谱系障碍(ASD)平均发病率为每 68 名儿童中就有 1 名(1.46%)。ASD 是一种多方面的神经发育障碍,也被认为是一种隐性残疾,因为在大多数情况下,ASD 儿童和正常发育儿童之间没有明显的形态差异。ASD 的诊断基于三个特征,包括社交障碍、语言障碍和重复刻板行为。儿科人群中 ASD 的发病率不断上升,且缺乏有效的治疗方法,这使得 ASD 成为医学上最具挑战性的疾病之一。ASD 神经生物学被认为与氧化应激有关,这表现为活性氧水平升高、脂质过氧化增加以及其他氧化应激指标增加。ASD 儿童被认为更容易受到氧化应激的影响,因为他们的细胞内和细胞外谷胱甘肽水平失衡,谷胱甘肽储备能力下降。多项研究表明,氧化还原失衡和氧化应激是 ASD 病理生理学的组成部分。因此,早期评估和治疗抗氧化状态可能会有更好的预后,因为它可以在氧化应激导致更多不可逆转的脑损伤之前,减少大脑中的氧化应激。在这篇综述中,考虑到氧化应激过程可能是治疗干预的靶点,讨论了氧化应激在 ASD 中的许多作用。