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Oxidative stress, metabolic and mitochondrial abnormalities associated with autism spectrum disorder.
Progress in Molecular Biology and Translational Science Pub Date : 2020-05-15 , DOI: 10.1016/bs.pmbts.2020.04.018
Morten Thorsen 1
Affiliation  

Autism spectrum disorder is a neurodevelopmental disorder characterized by impaired development and by abnormal function in regards to social interaction, communication and restricted, repetitive behavior. It affects approximately 1% of the worldwide population. Like other psychiatric disorders the diagnosis is based on observation of, and interview with the patient and next of kin, and diagnostic tests. Many genes have been associated with autism, but only few highly penetrant. Some researchers have instead focused on oxidative stress, metabolic abnormalities and mitochondrial dysfunction as an explanation of the disorder. Currently no cure exists for the disorder, making these abnormalities interesting as they are possibly correctable with supplements or treatment. These various processes cannot be seen independently as they are influencing and interacting with each other. Furthermore many of the metabolic changes seen in autism have also been shown in other psychiatric disorders such as attention deficit hyperactivity disorder, schizophrenia and bipolar disorder along with often comorbid disorders like epilepsy and intellectual disability. As such some of these abnormalities are not specific, however, could indicate a similar mechanism for the development of these disorders, with symptomatology and severity varying according to the location and the amount of damage done to proteins, cells and DNA. Clinical studies trying to treat these abnormalities, have widely been successful in correcting the metabolic abnormalities seen, but only some studies have also shown bettering of autistic symptoms. Hopefully with increased knowledge of the pathophysiology of the disorder, future preventive measures or treatment can be developed.



中文翻译:

与自闭症谱系障碍相关的氧化应激,代谢和线粒体异常。

自闭症谱系障碍是一种神经发育障碍,其特征是在社交互动,交流和受限的重复性行为方面发育受损和功能异常。它影响了全世界约1%的人口。像其他精神疾病一样,诊断基于对患者和近亲的观察,访谈以及诊断测试。许多基因与自闭症有关,但只有少数具有高度渗透性。相反,一些研究人员将注意力集中在氧化应激,代谢异常和线粒体功能障碍上,以此来解释这种疾病。目前尚无治愈该疾病的方法,使这些异常变得有趣,因为可以通过补充剂或治疗来纠正这些异常。这些不同的过程相互影响并相互作用,因此不能独立地看待。此外,在自闭症中发现的许多代谢变化也已在其他精神疾病中表现出来,例如注意力缺陷多动障碍,精神分裂症和躁郁症以及常见的合并症如癫痫和智力障碍。因此,这些异常中的一些不是特异性的,但是可能表明这些疾病发展的类似机制,其症状和严重程度会根据对蛋白质,细胞和DNA造成的损害的位置和受损程度而变化。尝试治疗这些异常的临床研究已广泛成功地纠正了所见到的代谢异常,但只有一些研究也显示出自闭症症状有所改善。

更新日期:2020-05-15
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